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Chen, Wuyan, Zhi Xu, Annie Sullivan, Gabriela P. Finkielstain, Carol Van Ryzin, Deborah P. Merke, and Nazli B. McDonnell. "Junction Site Analysis of Chimeric CYP21A1P/CYP21A2 Genes in 21-Hydroxylase Deficiency." Clinical Chemistry 58, no. 2 (February 1, 2012): 421–30. http://dx.doi.org/10.1373/clinchem.2011.174037.
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Abstract BACKGROUND Chimeric CYP21A1P/CYP21A2 genes, caused by homologous recombination between CYP21A2 (cytochrome P450, family 21, subfamily A, polypeptide 2) and its highly homologous pseudogene CYP21A1P (cytochrome P450, family 21, subfamily A, polypeptide 1 pseudogene), are common in patients with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency (21-OHD). A comprehensive junction site analysis of chimeric CYP21A1P/CYP21A2 genes is needed for optimizing genetic analysis strategy and determining clinical relevance. METHODS We conducted a comprehensive genetic analysis of chimeric CYP21A1P/CYP21A2 genes in a cohort of 202 unrelated 21-OHD patients. Targeted CYP21A2 mutation analysis was performed, and genotyping of chimeric CYP21A1P/CYP21A2 genes was cross-confirmed with Southern blot, RFLP, and multiplex ligation-dependent probe amplification analyses. Junction sites of chimera genes were determined by sequencing the long-PCR products amplified with primers CYP779f and Tena32F. An updated bioinformatics survey of Chi-like sequences was also performed. RESULTS Of 100 probands with a chimeric allele, 96 had a chimera associated with the severe classic salt-wasting form of CAH, and the remaining 4 carried an uncommon attenuated chimera with junction sites upstream of In2G (c.293–13A/C>G), which is associated with a milder phenotype. In addition to 6 of 7 reported chimeras, we identified a novel classic chimera (CH-8) and a novel attenuated chimera (CH-9). Attenuated chimeras explained prior genotype–phenotype discrepancies in 3 of the patients. Sequencing the CYP779f/Tena32F amplicons accurately differentiated between classic and attenuated chimeras. The bioinformatics survey revealed enrichment of Chi-like sequences within or in the vicinity of intron 2. CONCLUSIONS Junction site analysis can explain some genotype–phenotype discrepancies. Sequencing the well-established CYP779f/Tena32F amplicons is an unequivocal strategy for detecting attenuated chimeric CYP21A1P/CYP21A2 genes, which are clinically relevant.
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Sugawara, Kuniaki, Takumi Wakizuka, Atsushi Oowada, Takaya Moriguchi, and Mitsuo Omura. "Histogenic Identification by RAPD Analysis of Leaves and Fruit of Newly Synthesized Chimeric Citrus." Journal of the American Society for Horticultural Science 127, no. 1 (January 2002): 104–7. http://dx.doi.org/10.21273/jashs.127.1.104.
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Randomly amplified polymorphic DNA (RAPD) analysis was used to investigate the histogenic structure of leaf and fruit tissues in four graft chimeras, two intentional chimeras that were produced in combination with `Hamlin' orange [Citrus sinensis (L.) Osbeck] and `Satsuma' mandarin (C. unshiu Marc.), and two naturally occurring periclinal chimera cultivars, Kobayashi Mikan (a graft chimera of C. unshiu and C. natsudaidai Hayata), and Kinkoji Unshu (a graft chimera of C. unshiu and C. obovoidea hort. ex Takahashi). RAPD profiles of the lamina epidermis and the mesophyll cells of specific individuals indicated that the four graft chimeras were interspecific monekto chimeras, whose outermost layer (histogenic layer L-1) of the shoot apical meristem consisted of a species that was different from that in the inner layers (histogenic layers L-2 and L-3). Moreover, juice vesicles, which develop from the inside cells of the pericarp and become the main edible parts of Citrus fruit, were a mixture of the cells from both parental source cultivars. Therefore, the vesicles were at least composed of L-1 and subepidermal inner L-2 cells. This determination of interspecific chimeral construction (which was made possible by molecular techniques) is a valuable finding, in terms of improving Citrus through intentional use of periclinal chimerism.
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Kozikova, L., and E. Polteva. "New achievements in cell biology in poultry." Genetics and breeding of animals, no. 2 (August 26, 2022): 114–18. http://dx.doi.org/10.31043/2410-2733-2022-2-114-118.
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Purpose: development of new cell engineering in poultry farmingMaterials and methods. The following breeds of chickens were selected for research: Russian White, Minorca, Light Brahma and Fawn Brahma in comparison with the interspecific chimera of Japanese quail and Beijing duck. All chimeras were obtained by transplantation in the latter case of primary germ cells, in other breeds of blastodermal cells into the sub-embryonic region of recipient embryos. All embryonic cells before transplantation were cultivated for two days in special culture media supplemented with fetal cow serum and antibiotics. Chimeras were identified by the presence of contrasting feathers, unusual for this breed.Results. Unlike mammals, birds have a completely different embryonic development, which requires the development of new developments in cell biology to obtain chimeric birds. There are intrabreed chimeras and interspecies, obtained from organisms of different species. As an example of an interspecific chimera, a chimera of a Japanese quail and a Peking duck with a chimeric phenotype of black feathers on the neck is presented. Primary germ cells of Japanese quail served as donors. We obtained interbreeding chimeras of light and yellow brahma, when the donors were blastodermal cells of the light brahma, and the recipients were early embryos of the fawn brahma. Another variant of chimeras were chimeras between the breeds Russian White (donor blastodermal cells) and Minorca (embryo recipient).Conclusion. The observed sharp decline in the number of bird breeds requires new approaches to their conservation and the creation of new genetic organisms. With the help of modern developments in cell biology, it has become possible to create a new strategy for obtaining chimeric birds. The use of pluripotent embryonic cells has led to the creation of interbreed and interspecies bird chimeras.
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Ebrahimzadeh, P., M. Schiek, P. Jaros, T. Kapitaniak, S. van Waasen, and Y. Maistrenko. "Minimal chimera states in phase-lag coupled mechanical oscillators." European Physical Journal Special Topics 229, no. 12-13 (September 2020): 2205–14. http://dx.doi.org/10.1140/epjst/e2020-900270-4.
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Abstract We obtain experimental chimera states in the minimal network of three identical mechanical oscillators (metronomes), by introducing phase-lagged all-to-all coupling. For this, we have developed a real-time model-in-the-loop coupling mechanism that allows for flexible and online change of coupling topology, strength and phase-lag. The chimera states manifest themselves as a mismatch of average frequency between two synchronous and one desynchronized oscillator. We find this kind of striking “chimeric” behavior is robust in a wide parameter region. At other parameters, however, chimera state can lose stability and the system behavior manifests itself as a heteroclinic switching between three saddle-type chimeras. Our experimental observations are in a qualitative agreement with the model simulation.
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Slack, Jeffrey M., Edward M. Dougherty, and Susan D. Lawrence. "A study of the Autographa californica multiple nucleopolyhedrovirus ODV envelope protein p74 using a GFP tag." Journal of General Virology 82, no. 9 (September 1, 2001): 2279–87. http://dx.doi.org/10.1099/0022-1317-82-9-2279.
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The Autographa californica multiple nucleopolyhedrovirus (AcMNPV) protein p74 is associated with the occlusion-derived virus (ODV) envelope. p74 is essential for oral infectivity of ODV and has been proposed to play a role in midgut attachment and/or fusion. In this study, p74 protein was expressed in-frame with green fluorescent protein (GFP) to create a p74–GFP chimera. The C-terminal GFP portion of the chimera facilitated visualization of the trafficking of p74 in baculovirus-infected Spodoptera frugiperda (Sf-9) cells. p74–GFP chimeric proteins localized in the intranuclear ring zone of the nucleus and were found to co-precipitate with the microvesicle fraction of cell lysates. A series of truncations of p74 was expressed as p74–GFP chimeras in recombinant baculoviruses. When C-terminal region S580–F645 was deleted from p74, p74–GFP chimera localization became non-specific and chimeras became soluble. p74 region S580–F645 directed GFP to the intranuclear ring zone in a similar pattern to full-length p74. The hydrophobic C terminus of p74 plays a role in protein localization and possibly in transmembrane anchoring and insertion.
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Zakharova, Anna, Marie Kapeller, and Eckehard Schöll. "Amplitude chimeras and chimera death in dynamical networks." Journal of Physics: Conference Series 727 (June 2016): 012018. http://dx.doi.org/10.1088/1742-6596/727/1/012018.
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Wataghin, Lucia. "La Chimera di Dino Campana e Altre Chimere." Revista de Italianística, no. 16 (August 30, 2008): 37. http://dx.doi.org/10.11606/issn.2238-8281.v0i16p37-43.
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Patidar, Manoj, Naveen Yadav, and Sarat K. Dalai. "Influence of Length and Amino Acid Composition on Dimer Formation of Immunoglobulin based Chimera." Current Pharmaceutical Design 24, no. 11 (June 27, 2018): 1211–23. http://dx.doi.org/10.2174/1381612823666171018115206.
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Background: The dimeric immunoglobulin (Ig) chimeras used for drug targeting and delivery are preferred biologics over their monomeric forms. Designing these Ig chimeras involves critical selection of a suitable Ig base that ensures dimer formation. In the present study, we systematically analyzed several factors that influence the formation of dimeric chimera. We designed and predicted 608 cytokine-Ig chimeras where we tested the contributions of (1) different domains of Ig constant heavy chain, (2) length of partner proteins, (3) amino acid (AA) composition and (4) position of cysteine in the formation of homodimer. Method: The sequences of various Ig and cytokines were procured from Uniprot database, fused and submitted to COTH (CO-THreader) server for the prediction of dimer formation. Contributions of different domains of Ig constant heavy chain, length of chimeric proteins, AA composition and position of cysteine to the homodimer formation of 608 cytokine-Ig chimeras were tested. Various in silico approaches were adopted for validating the in silico findings. Experimentally we also validated our approach by expressing the chimeric design of shorter cytokine with Ig domain in CHO cells and analyzing the protein by SDS-PAGE. Results: Our results advocate that while the CH1 region and the Hinge region of Ig heavy chain are critical, the length of partner proteins also crucially influences homodimer formation of the Ig-based chimera. We also report that the CH1 domain of Ig is not required for dimer formation of Ig based chimera in the presence of larger partner proteins. For shorter partner proteins fused to CH2-CH3, careful selection of partner sequence is critical, particularly the hydrophobic AA composition, cysteine content & their positions, disulphide bond formation property, and the linker sequences. We validated our in silico observation by various bioinformatics tools and checked the ability of chimeras to bind with the receptors of native protein by docking studies. As a proof of concept, we have expressed the chimeric proteins in CHO cells and found that our design favors the synthesis of dimeric proteins. Conclusion: Our structural prediction study suggests that extra amino acids in the range of 15-20 added to the CH2 domain of Ig is a critical requirement to make homodimer. This information from our study will have implication in designing efficacious homodimeric chimera.
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Pham, Quynh N., Stéphane Biacchesi, Mario H. Skiadopoulos, Brian R. Murphy, Peter L. Collins, and Ursula J. Buchholz. "Chimeric Recombinant Human Metapneumoviruses with the Nucleoprotein or Phosphoprotein Open Reading Frame Replaced by That of Avian Metapneumovirus Exhibit Improved Growth In Vitro and Attenuation In Vivo." Journal of Virology 79, no. 24 (December 15, 2005): 15114–22. http://dx.doi.org/10.1128/jvi.79.24.15114-15122.2005.
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ABSTRACT Chimeric versions of recombinant human metapneumovirus (HMPV) were generated by replacing the nucleoprotein (N) or phosphoprotein (P) open reading frame with its counterpart from the closely related avian metapneumovirus (AMPV) subgroup C. In Vero cells, AMPV replicated to an approximately 100-fold-higher titer than HMPV. Surprisingly, the N and P chimeric viruses replicated to a peak titer that was 11- and 25-fold higher, respectively, than that of parental HMPV. The basis for this effect is not known but was not due to obvious changes in the efficiency of gene expression. AMPV and the N and P chimeras were evaluated for replication, immunogenicity, and protective efficacy in hamsters. AMPV was attenuated compared to HMPV in this mammalian host on day 5 postinfection, but not on day 3, and only in the nasal turbinates. In contrast, the N and P chimeras were reduced approximately 100-fold in both the upper and lower respiratory tract on day 3 postinfection, although there was little difference by day 5. The N and P chimeras induced a high level of neutralizing serum antibodies and protective efficacy against HMPV; AMPV was only weakly immunogenic and protective against HMPV challenge, reflecting antigenic differences. In African green monkeys immunized intranasally and intratracheally, the mean peak titer of the P chimera was reduced 100- and 1,000-fold in the upper and lower respiratory tracts, whereas the N chimera was reduced only 10-fold in the lower respiratory tract. Both chimeras were comparable to wild-type HMPV in immunogenicity and protective efficacy. Thus, the P chimera is a promising live HMPV vaccine candidate that paradoxically combines improved growth in vitro with attenuation in vivo.
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Cairns, Tina M., Richard S. B. Milne, Manuel Ponce-de-Leon, Deanna K. Tobin, Gary H. Cohen, and Roselyn J. Eisenberg. "Structure-Function Analysis of Herpes Simplex Virus Type 1 gD and gH-gL: Clues from gDgH Chimeras." Journal of Virology 77, no. 12 (June 15, 2003): 6731–42. http://dx.doi.org/10.1128/jvi.77.12.6731-6742.2003.
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ABSTRACT In alphaherpesviruses, glycoprotein B (gB), gD, gH, and gL are essential for virus entry. A replication-competent gL-null pseudorabies virus (PrV) (B. G. Klupp and T. C. Mettenleiter, J. Virol. 73:3014-3022, 1999) was shown to express a gDgH hybrid protein that could replace gD, gH, and gL in cell-cell fusion and null virus complementation assays. To study this phenomenon in herpes simplex virus type 1 (HSV-1), we constructed four gDgH chimeras, joining the first 308 gD amino acids to various gH N-terminal truncations. The chimeras were named for the first amino acid of gH at which each was truncated: 22, 259, 388, and 432. All chimeras were immunoprecipitated with both gD and gH antibodies to conformational epitopes. Normally, transport of gH to the cell surface requires gH-gL complex formation. Chimera 22 contains full-length gH fused to gD308. Unlike PrV gDgH, chimera 22 required gL for transport to the surface of transfected Vero cells. Interestingly, although chimera 259 failed to reach the cell surface, chimeras 388 and 432 exhibited gL-independent transport. To examine gD and gH domain function, each chimera was tested in cell-cell fusion and null virus complementation assays. Unlike PrV gDgH, none of the HSV-1 chimeras substituted for gL for fusion. Only chimera 22 was able to replace gH for fusion and could also replace either gH or gD in the complementation assay. Surprisingly, this chimera performed very poorly as a substitute for gD in the fusion assay despite its ability to complement gD-null virus and bind HSV entry receptors (HveA and nectin-1). Chimeras 388 and 432, which contain the same portion of gD as that in chimera 22, substituted for gD for fusion at 25 to 50% of wild-type levels. However, these chimeras functioned poorly in gD-null virus complementation assays. The results highlight the fact that these two functional assays are measuring two related but distinct processes.
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Aras, Emekcan, Stéphane Delbruel, Fan Yang, Wouter Joosen, and Danny Hughes. "Chimera." ACM Transactions on Internet of Things 2, no. 2 (May 2021): 1–25. http://dx.doi.org/10.1145/3440995.
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The Internet of Things (IoT) is being deployed in an ever-growing range of applications, from industrial monitoring to smart buildings to wearable devices. Each of these applications has specific computational requirements arising from their networking, system security, and edge analytics functionality. This diversity in requirements motivates the need for adaptable end-devices, which can be re-configured and re-used throughout their lifetime to handle computation-intensive tasks without sacrificing battery lifetime. To tackle this problem, this article presents Chimera, a low-power platform for research and experimentation with reconfigurable hardware for the IoT end-devices. Chimera achieves flexibility and re-usability through an architecture based on a Flash Field Programmable Gate Array (FPGA) with a reconfigurable software stack that enables over-the-air hardware and software evolution at runtime. This adaptability enables low-cost hardware/software upgrades on the end-devices and an increased ability to handle computationally-intensive tasks. This article describes the design of the Chimera hardware platform and software stack, evaluates it through three application scenarios, and reviews the factors that have thus far prevented FPGAs from being utilized in IoT end-devices.
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Paredes, Luis, Caroline McMillan, Wan Kyn Chan, Senthil Chandrasegaran, Ramyak Singh, Karthik Ramani, and Danielle Wilde. "CHIMERA." Proceedings of the ACM on Interactive, Mobile, Wearable and Ubiquitous Technologies 5, no. 4 (December 27, 2021): 1–24. http://dx.doi.org/10.1145/3494974.
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Wearable technologies draw on a range of disciplines, including fashion, textiles, HCI, and engineering. Due to differences in methodology, wearables researchers can experience gaps or breakdowns in values, goals, and vocabulary when collaborating. This situation makes wearables development challenging, even more so when technologies are in the early stages of development and their technological and cultural potential is not fully understood. We propose a common ground to enhance the accessibility of wearables-related resources. The objective is to raise awareness and create a convergent space for researchers and developers to both access and share information across domains. We present CHIMERA, an online search interface that allows users to explore wearable technologies beyond their discipline. CHIMERA is powered by a Wearables Taxonomy and a database of research, tutorials, aesthetic approaches, concepts, and patents. To validate CHIMERA, we used a design task with multidisciplinary designers, an open-ended usability study with experts, and a usability survey with students of a wearables design class. Our findings suggest that CHIMERA assists users with different mindsets and skillsets to engage with information, expand and share knowledge when developing wearables. It forges common ground across divergent disciplines, encourages creativity, and affords the formation of inclusive, multidisciplinary perspectives in wearables development.
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Lee, Dongyoon, Peter M. Chen, Jason Flinn, and Satish Narayanasamy. "Chimera." ACM SIGPLAN Notices 47, no. 6 (August 6, 2012): 463–74. http://dx.doi.org/10.1145/2345156.2254119.
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Park, Jason Jong Kyu, Yongjun Park, and Scott Mahlke. "Chimera." ACM SIGPLAN Notices 50, no. 4 (May 12, 2015): 593–606. http://dx.doi.org/10.1145/2775054.2694346.
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Park, Jason Jong Kyu, Yongjun Park, and Scott Mahlke. "Chimera." ACM SIGARCH Computer Architecture News 43, no. 1 (May 29, 2015): 593–606. http://dx.doi.org/10.1145/2786763.2694346.
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Anderson, Kenneth M., Richard N. Taylor, and E. James Whitehead. "Chimera." ACM Transactions on Information Systems 18, no. 3 (July 2000): 211–45. http://dx.doi.org/10.1145/352595.352596.
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Sun, Chong, Narasimhan Rampalli, Frank Yang, and AnHai Doan. "Chimera." Proceedings of the VLDB Endowment 7, no. 13 (August 2014): 1529–40. http://dx.doi.org/10.14778/2733004.2733024.
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Taylor, Richard, and David Redmiles. "Chimera." ACM SIGSOFT Software Engineering Notes 25, no. 1 (January 2000): 98. http://dx.doi.org/10.1145/340855.341074.
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Li, Joan. "Chimera." New England Review 39, no. 4 (2018): 55–65. http://dx.doi.org/10.1353/ner.2018.0110.
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Piller, K. J., C. J. Decker, L. N. Rusché, and B. Sollner-Webb. "Trypanosoma brucei mitochondrial guide RNA-mRNA chimera-forming activity cofractionates with an editing-domain-specific endonuclease and RNA ligase and is mimicked by heterologous nuclease and RNA ligase." Molecular and Cellular Biology 15, no. 6 (June 1995): 2925–32. http://dx.doi.org/10.1128/mcb.15.6.2925.
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RNA editing in trypanosomes has been proposed to occur through transesterification or endonuclease cleavage and RNA ligation reactions. Both models involve a chimeric intermediate in which a guide RNA (gRNA) is joined through its 3' oligo(U) tail to an editing site of the corresponding mRNA. Velocity centrifugation of Trypanosoma brucei mitochondrial extracts had been reported to completely separate the gRNA-mRNA chimera-forming activity from endonuclease activity (V. W. Pollard, M. E. Harris, and S. L. Hajduk, EMBO J. 11:4429-4438, 1992), appearing to rule out the endonuclease-RNA ligase mechanism. However, we show that an editing-domain-specific endonuclease activity does cosediment with the chimera-forming activity, as does the RNA ligase activity, but detection of the specific endonuclease requires reducing assay conditions. This report further demonstrates that the T. brucei chimera-forming activity is mimicked by mung bean nuclease and T4 RNA ligase. Using cytochrome b (CYb) preedited mRNA and a model CYb gRNA, we found that these heterologous enzymes specifically generate CYb gRNA-mRNA chimeras analogous to those formed in the mitochondrial extract. These combined results provide support for the endonuclease-RNA ligase mechanism of chimera formation.
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Mathews, P. M., J. B. Martinie, and D. M. Fambrough. "The pathway and targeting signal for delivery of the integral membrane glycoprotein LEP100 to lysosomes." Journal of Cell Biology 118, no. 5 (September 1, 1992): 1027–40. http://dx.doi.org/10.1083/jcb.118.5.1027.
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A complete set of chimeras was made between the lysosomal membrane glycoprotein LEP100 and the plasma membrane-directed vesicular stomatitis virus G protein, combining a glycosylated lumenal or ectodomain, a single transmembrane domain, and a cytosolic carboxyl-terminal domain. These chimeras, the parent molecules, and a truncated form of LEP100 lacking the transmembrane and cytosolic domains were expressed in mouse L cells. Only LEP100 and chimeras that included the cytosolic 11 amino acid carboxyl terminus of LEP100 were targeted to lysosomes. The other chimeras accumulated in the plasma membrane, and truncated LEP100 was secreted. Chimeras that included the extracellular domain of vesicular stomatitis G protein and the carboxyl terminus of LEP100 were targeted to lysosomes and very rapidly degraded. Therefore, in chimera-expressing cells, virtually all the chimeric molecules were newly synthesized and still in the biosynthesis and lysosomal targeting pathways. The behavior of one of these chimeras was studied in detail. After its processing in the Golgi apparatus, the chimera entered the plasma membrane/endosome compartment and rapidly cycled between the plasma membrane and endosomes before going to lysosomes. In pulse-expression experiments, a large population of chimeric molecules was observed to appear transiently in the plasma membrane by immunofluorescence microscopy. Soon after protein synthesis was inhibited, this surface population disappeared. When lysosomal proteolysis was inhibited, chimeric molecules accumulated in lysosomes. These data suggest that the plasma membrane/early endosome compartment is on the pathway to the lysosomal membrane. This explains why mutations that block endocytosis result in the accumulation of lysosomal membrane proteins in the plasma membrane.
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Thomas, Eleanor V., Wayne A. Fenton, James McGrath, and Arthur L. Horwich. "Transfer of pathogenic and nonpathogenic cytosolic proteins between spinal cord motor neurons in vivo in chimeric mice." Proceedings of the National Academy of Sciences 114, no. 15 (March 27, 2017): E3139—E3148. http://dx.doi.org/10.1073/pnas.1701465114.
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Recent studies have reported spread of pathogenic proteins in the mammalian nervous system, but whether nonpathogenic ones spread is unknown. We initially investigated whether spread of a mutant amyotrophic lateral sclerosis-associated cytosolic superoxide dismutase 1 (SOD1) protein between motor neurons could be detected in intact chimeric mice. Eight-cell embryos from G85R SOD1YFP and G85R SOD1CFP mice were aggregated, and spinal cords of adult chimeric progeny were examined for motor neurons with cytosolic double fluorescence. By 3 mo of age, we observed extensive double fluorescence, including in amyotrophic lateral sclerosis-affected cranial nerve motor nuclei but not in the relatively spared extraocular nuclei. Chimeras of nonpathogenic wtSOD1YFP and G85R SOD1CFP also exhibited double fluorescence. In a third chimera, mitochondrial mCherry did not transfer to G85R SOD1YFP motor neurons, suggesting that neither RNA nor organelles transfer, but mito-mCherry neurons received G85R SOD1YFP. In a chimera of ChAT promoter-EGFP and mito-mCherry, EGFP efficiently transferred to mito-mCherry+ cells. Thus, nonpathogenic cytosolic proteins appear capable of transfer. During study of both the SOD1FP and EGFP chimeras, we observed fluorescence also in small cells neighboring the motor neurons, identified as mature gray matter oligodendrocytes. Double fluorescence in the G85R SOD1FP chimera and observation of the temporal development of fluorescence first in motor neurons and then in these oligodendrocytes suggest that they may be mediators of transfer of cytosolic proteins between motor neurons.
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Koenderink, Jan B., Herman G. P. Swarts, H. Christiaan Stronks, Harm P. H. Hermsen, Peter H. G. M. Willems, and Jan Joep H. H. M. De Pont. "Chimeras of X+,K+-ATPases." Journal of Biological Chemistry 276, no. 15 (January 16, 2001): 11705–11. http://dx.doi.org/10.1074/jbc.m010804200.
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In this study we reveal regions of Na+,K+-ATPase and H+,K+-ATPase that are involved in cation selectivity. A chimeric enzyme in which transmembrane hairpin M5-M6 of H+,K+-ATPase was replaced by that of Na+,K+-ATPase was phosphorylated in the absence of Na+and showed no K+-dependent reactions. Next, the part originating from Na+,K+-ATPase was gradually increased in the N-terminal direction. We demonstrate that chimera HN16, containing the transmembrane segments one to six and intermediate loops of Na+,K+-ATPase, harbors the amino acids responsible for Na+specificity. Compared with Na+,K+-ATPase, this chimera displayed a similar apparent Na+affinity, a lower apparent K+affinity, a higher apparent ATP affinity, and a lower apparent vanadate affinity in the ATPase reaction. This indicates that theE2K form of this chimera is less stable than that of Na+,K+-ATPase, suggesting that it, like H+,K+-ATPase, de-occludes K+ions very rapidly. Comparison of the structures of these chimeras with those of the parent enzymes suggests that the C-terminal 187 amino acids and the β-subunit are involved in K+occlusion. Accordingly, chimera HN16 is not only a chimeric enzyme in structure, but also in function. On one hand it possesses the Na+-stimulated ATPase reaction of Na+,K+-ATPase, while on the other hand it has the K+occlusion properties of H+,K+-ATPase.
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Rusché, L. N., K. J. Piller, and B. Sollner-Webb. "Guide RNA-mRNA chimeras, which are potential RNA editing intermediates, are formed by endonuclease and RNA ligase in a trypanosome mitochondrial extract." Molecular and Cellular Biology 15, no. 6 (June 1995): 2933–41. http://dx.doi.org/10.1128/mcb.15.6.2933.
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RNA editing in kinetoplast mitochondrial transcripts involves the insertion and/or deletion of uridine residues and is directed by guide RNAs (gRNAs). It is thought to occur through a chimeric intermediate in which the 3' oligo(U) tail of the gRNA is covalently joined to the 3' portion of the mRNA at the site being edited. Chimeras have been proposed to be formed by a transesterification reaction but could also be formed by the known mitochondrial site-specific nuclease and RNA ligase. To distinguish between these models, we studied chimera formation in vitro directed by a trypanosome mitochondrial extract. This reaction was found to occur in two steps. First, the mRNA is cleaved in the 3' portion of the editing domain, and then the 3' fragment derived from this cleavage is ligated to the gRNA. The isolated mRNA 3' cleavage product is a more efficient substrate for chimera formation than is the intact mRNA, inconsistent with a transesterification mechanism but supporting a nuclease-ligase mechanism. Also, when normal mRNA cleavage is inhibited by the presence of a phosphorothioate, normal chimera formation no longer occurs. Rather, this phosphorothioate induces both cleavage and chimera formation at a novel site within the editing domain. Finally, levels of chimera-forming activity correlate with levels of mitochondrial RNA ligase activity when reactions are conducted under conditions which inhibit the ligase, including the lack of ATP containing a cleavable alpha-beta bond. These data show that chimera formation in the mitochondrial extract occurs by a nuclease-ligase mechanism rather than by transesterification.
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Ramos, Jorge, Wonyong Jung, Josefina Ramos-Franco, Gregory A. Mignery, and Michael Fill. "Single Channel Function of Inositol 1,4,5-trisphosphate Receptor Type-1 and -2 Isoform Domain-Swap Chimeras." Journal of General Physiology 121, no. 5 (April 14, 2003): 399–411. http://dx.doi.org/10.1085/jgp.200208718.
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The InsP3R proteins have three recognized domains, the InsP3-binding, regulatory/coupling, and channel domains (Mignery, G.A., and T.C. Südhof. 1990. EMBO J. 9:3893–3898). The InsP3 binding domain and the channel-forming domain are at opposite ends of the protein. Ligand regulation of the channel must involve communication between these different regions of the protein. This communication likely involves the interceding sequence (i.e., the regulatory/coupling domain). The single channel functional attributes of the full-length recombinant type-1, -2, and -3 InsP3R channels have been defined. Here, two type-1/type-2 InsP3R regulatory/coupling domain chimeras were created and their single channel function defined. One chimera (1-2-1) contained the type-2 regulatory/coupling domain in a type-1 backbone. The other chimera (2-1-2) contained the type-1 regulatory/coupling domain in a type-2 backbone. These chimeric proteins were expressed in COS cells, isolated, and then reconstituted in proteoliposomes. The proteoliposomes were incorporated into artificial planar lipid bilayers and the single-channel function of the chimeras defined. The chimeras had permeation properties like that of wild-type channels. The ligand regulatory properties of the chimeras were altered. The InsP3 and Ca2+ regulation had some unique features but also had features in common with wild-type channels. These results suggest that different independent structural determinants govern InsP3R permeation and ligand regulation. It also suggests that ligand regulation is a multideterminant process that involves several different regions of the protein. This study also demonstrates that a chimera approach can be applied to define InsP3R structure-function.
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Wang, Chin-Tien, Yen-Chiou Chou, and Chien-Cheng Chiang. "Assembly and Processing of Human Immunodeficiency Virus Gag Mutants Containing a Partial Replacement of the Matrix Domain by the Viral Protease Domain." Journal of Virology 74, no. 7 (April 1, 2000): 3418–22. http://dx.doi.org/10.1128/jvi.74.7.3418-3422.2000.
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ABSTRACT We constructed human immunodeficiency virus (HIV) mutants by replacing the matrix domain with sequences encoding the viral protease or p6* and protease. The chimeras retaining matrix myristylation and processing signals underwent efficient autoprocessing with severely defective particle budding. The budding defects of the chimeras were rescued by suppressing the chimera protease activity either through addition of an HIV protease inhibitor or through inactivating the chimera protease via a substitution mutation of the catalytic aspartic acid residue. This resulted in the release of chimeric virus-like particles with the density of a wild-type retrovirus particle. In addition, the assembly-competent but processing-defective chimeras produced proteolytically processed particles with significant reverse transcriptase activity when a downstream native pol gene was present. These results suggest that HIV has the potential to adapt heterologous sequences in place of the matrix sequence without major effects on virus-like particle budding. In addition, the positions of the protease and substrate accessibility may contribute significantly toward avoiding a premature Gag or Gag-Pol process, which leads to severe defects in both particle budding and incorporation.
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Li, Ming-yin. "Observation of High-frequency Occurrence of Chimeral Adventitious Shoots in Tissue Culture from the Chimeral Tissues of Pelargonium zonale." HortScience 40, no. 5 (August 2005): 1461–63. http://dx.doi.org/10.21273/hortsci.40.5.1461.
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In Pelargonium, the plastid mutation in three independent cell layers L1, L2, and L3, can produce plastid chimeras with visible shoot colour difference such as GWG (green-white-green) and GGW (green-green-white). Chimera can be used to trace the relationship between the cell layers of different genotypes during shoot development and the effect of the mutated genes on shoot development. In this study, we have obtained different adventitious shoots with GGG, GWG, GGW, and WWW combinations of cell layers through tissue culture of petioles and internodes from GGW and GWG chimeras of Pelargonium zonale `Mrs Pollock'. Much higher percentage (14.9%) of chimeral adventitious shoots was obtained from GGW tissues than from GWG tissues (4.2%). Of the 10.8% chimeral adventitious shoots regenerated in this experiment, 8.6% are different from the original type of explants. This result indicated that cells at least in both L2 and L3 of the explants were involved in the regeneration of the adventitious shoots. The number of shoot types regenerated is likely dependent on the number and the type of cells that were in direct contact with the culture medium. It is suggested that the mixed cells can be used to produce the chimera by tissue culture. Three possible ways to form the chimeras in vitro culture were discussed. Chemical names used: TDZ =1-phenyl-3-(1,2,3-thiadiazol-5-yl)urea (Thidiazuron); IAA = Indole-3-acetic acid; PVP = polyvinylpyrrolidone.
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Lee, Seyoung, Jiye Lee, and Jehee Lee. "Learning Virtual Chimeras by Dynamic Motion Reassembly." ACM Transactions on Graphics 41, no. 6 (November 30, 2022): 1–13. http://dx.doi.org/10.1145/3550454.3555489.
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The Chimera is a mythological hybrid creature composed of different animal parts. The chimera's movements are highly dependent on the spatial and temporal alignments of its composing parts. In this paper, we present a novel algorithm that creates and animates chimeras by dynamically reassembling source characters and their movements. Our algorithm exploits a two-network architecture: part assembler and dynamic controller. The part assembler is a supervised learning layer that searches for the spatial alignment among body parts, assuming that the temporal alignment is provided. The dynamic controller is a reinforcement learning layer that learns robust control policy for a wide variety of potential temporal alignments. These two layers are tightly intertwined and learned simultaneously. The chimera animation generated by our algorithm is energy efficient and expressive in terms of describing weight shifting, balancing, and full-body coordination. We demonstrate the versatility of our algorithm by generating the motor skills of a large variety of chimeras from limited source characters.
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Mysara, Mohamed, Yvan Saeys, Natalie Leys, Jeroen Raes, and Pieter Monsieurs. "CATCh, an Ensemble Classifier for Chimera Detection in 16S rRNA Sequencing Studies." Applied and Environmental Microbiology 81, no. 5 (December 19, 2014): 1573–84. http://dx.doi.org/10.1128/aem.02896-14.
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ABSTRACTIn ecological studies, microbial diversity is nowadays mostly assessed via the detection of phylogenetic marker genes, such as 16S rRNA. However, PCR amplification of these marker genes produces a significant amount of artificial sequences, often referred to as chimeras. Different algorithms have been developed to remove these chimeras, but efforts to combine different methodologies are limited. Therefore, two machine learning classifiers (reference-based andde novoCATCh) were developed by integrating the output of existing chimera detection tools into a new, more powerful method. When comparing our classifiers with existing tools in either the reference-based orde novomode, a higher performance of our ensemble method was observed on a wide range of sequencing data, including simulated, 454 pyrosequencing, and Illumina MiSeq data sets. Since our algorithm combines the advantages of different individual chimera detection tools, our approach produces more robust results when challenged with chimeric sequences having a low parent divergence, short length of the chimeric range, and various numbers of parents. Additionally, it could be shown that integrating CATCh in the preprocessing pipeline has a beneficial effect on the quality of the clustering in operational taxonomic units.
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Polejaeva, Irina, and Shoukhrat Mitalipov. "Stem cell potency and the ability to contribute to chimeric organisms." REPRODUCTION 145, no. 3 (March 2013): R81—R88. http://dx.doi.org/10.1530/rep-12-0396.
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Mouse embryonic chimeras are a well-established tool for studying cell lineage commitment and pluripotency. Experimental chimeras were successfully produced by combining two or more preimplantation embryos or by introducing into host embryo cultured pluripotent embryonic stem cells (ESCs). Chimera production using genetically modified ESCs became the method of choice for the generation of knockout or knockin mice. Although the derivation of ESCs or ESC-like cells has been reported for other species, only mouse and rat pluripotent stem cells have been shown to contribute to germline-competent chimeras, which is the defining feature of ESCs. Herein, we describe different approaches employed for the generation of embryonic chimeras, define chimera-competent cell types, and describe cases of spontaneous chimerism in humans. We also review the current state of derivation of pluripotent stem cells in several species and discuss outcomes of various chimera studies when such cells are used.
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Esawi, Ezaldeen, Walhan Alshaer, Ismail Sami Mahmoud, Dana A. Alqudah, Bilal Azab, and Abdalla Awidi. "Aptamer-Aptamer Chimera for Targeted Delivery and ATP-Responsive Release of Doxorubicin into Cancer Cells." International Journal of Molecular Sciences 22, no. 23 (November 30, 2021): 12940. http://dx.doi.org/10.3390/ijms222312940.
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Aptamers offer a great opportunity to develop innovative drug delivery systems that can deliver cargos specifically into targeted cells. In this study, a chimera consisting of two aptamers was developed to deliver doxorubicin into cancer cells and release the drug in cytoplasm in response to adenosine-5′-triphosphate (ATP) binding. The chimera was composed of the AS1411 anti-nucleolin aptamer for cancer cell targeting and the ATP aptamer for loading and triggering the release of doxorubicin in cells. The chimera was first produced by hybridizing the ATP aptamer with its complementary DNA sequence, which is linked with the AS1411 aptamer via a poly-thymine linker. Doxorubicin was then loaded inside the hybridized DNA region of the chimera. Our results show that the AS1411–ATP aptamer chimera was able to release loaded doxorubicin in cells in response to ATP. In addition, selective uptake of the chimera into cancer cells was demonstrated using flow cytometry. Furthermore, confocal laser scanning microscopy showed the successful delivery of the doxorubicin loaded in chimeras to the nuclei of targeted cells. Moreover, the doxorubicin-loaded chimeras effectively inhibited the growth of cancer cell lines and reduced the cytotoxic effect on the normal cells. Overall, the results of this study show that the AS1411–ATP aptamer chimera could be used as an innovative approach for the selective delivery of doxorubicin to cancer cells, which may improve the therapeutic potency and decrease the off-target cytotoxicity of doxorubicin.
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Meena, Chandrakala, K. Murali, and Sudeshna Sinha. "Chimera States in Star Networks." International Journal of Bifurcation and Chaos 26, no. 09 (August 2016): 1630023. http://dx.doi.org/10.1142/s0218127416300238.
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We consider star networks of chaotic oscillators, with all end-nodes connected only to the central hub node, under diffusive coupling, conjugate coupling and mean-field diffusive coupling. We observe the existence of chimeras in the end-nodes, which are identical in terms of the coupling environment and dynamical equations. Namely, the symmetry of the end-nodes is broken and coexisting groups with different synchronization features and attractor geometries emerge. Surprisingly, such chimera states are very wide-spread in this network topology, and large parameter regimes of moderate coupling strengths evolve to chimera states from generic random initial conditions. Further, we verify the robustness of these chimera states in analog circuit experiments. Thus it is evident that star networks provide a promising class of coupled systems, in natural or engineered contexts, where chimeras are prevalent.
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Evenäs, Petra, Pablo García de Frutos, Gerry Nicolaes, and Björn Dahlbäck. "The Second Laminin G-type Domain of Protein S Is Indispensable for Expression of Full Cofactor Activity in Activated Protein C-catalysed Inactivation of Factor Va and Factor VIIIa." Thrombosis and Haemostasis 84, no. 08 (2000): 271–77. http://dx.doi.org/10.1055/s-0037-1614007.
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SummaryVitamin K-dependent protein S is a cofactor to the anticoagulant serine protease activated protein C (APC) in the proteolytic inactivation of the procoagulant, activated factor V (FVa) and factor VIII (FVIIIa). In the FVa degradation, protein S selectively accelerates the cleavage at Arg306, having no effect on the Arg506 cleavage. In the FVIIIa inactivation, the APC-cofactor activity of protein S is synergistically potentiated by FV, which thus has the capacity to function both as a pro- and an anticoagulant protein. The SHBG-like region of protein S, containing two laminin G-type domains, is required for the combined action of protein S and FV. To elucidate whether both G domains in protein S are needed for expression of APC-cofactor activities, chimeras of human protein S were created in which the individual G domains were replaced by the corresponding domain of the homologous Gas6, which in itself has no anticoagulant activity. In a plasmabased assay, chimera I (G1 from Gas6) was as efficient as wild-type recombinant protein S, whereas chimera II (G2 from Gas6) was less effective. The synergistic cofactor activity with FV in the inactivation of FVIIIa was lost by the replacement of the G2 domain in protein S (chimera II). However, chimera I did not exert full APC-cofactor activity in the FVIIIa degradation, indicating involvement of both G domains or the entire SHBG-like region in this reaction. Chimera I was fully active in the degradation of FVa in contrast to chimera II, which exhibited reduced cofactor activity compared to protein S. In conclusion, by using protein S-Gas6 chimeric proteins, we have identified the G2 domain of protein S to be indispensable for an efficient inactivation of both FVIIIa and FVa, whereas the G1 domain was found not to be of direct importance in the FVa-inactivation experiments.
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Player, RK Maitra, RH Silverman, and PF Torrence. "Targeting RNase L to Human Immunodeficiency Virus RNA with 2-5A-Antisense." Antiviral Chemistry and Chemotherapy 9, no. 3 (June 1998): 225–31. http://dx.doi.org/10.1177/095632029800900303.
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In an attempt to develop a lead for the application of 2–5A-antisense to the targeted destruction of human immunodeficiency virus (HIV) RNA, specific target sequences within the HIV mRNAs were identified by analysis of the theoretical secondary structure. 2-5A-antisense chimeras were chosen against a total of 11 different sequences: three in the gag mRNA, three in the rev mRNA and five in the tat mRNA. 2-5A-antisense chimera synthesis was accomplished using solid-phase phosphoramidite chemistry. These chimeras were evaluated for their activity in a cell-free assay system using purified recombinant human RNase L to effect cleavage of 32P-labelled RNA transcripts of plasmids derived from HIV NL4-3. This screening revealed that of the three 2-5A-antisense chimeras targeted against gag mRNA, only one had significant HIV RNA cleavage activity, approximately10-fold-reduced compared to the parent 2-5A tetramer and comparable to that reported for the prototypical 2-5A-anti-PKR chimera, targeted against PKR mRNA. The cleavage activity of this chimera was specific, since a scrambled antisense domain chimera and a chimera without the key 5′-monophosphate moiety were both inactive. The 10 other 2-5A-antisense chimeras against tat and rev had significantly less activity. These results imply that HIV gag RNA, like PKR RNA and a model HIV tat-oligoA- vif RNA, can be cleaved using the 2-5A-antisense approach. The results further imply that not all regions of a potential RNA target are accessible to the 2-5A-antisense approach.
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Lekcharoensuk, Porntippa, Igor Morozov, Prem S. Paul, Nattarat Thangthumniyom, Worawidh Wajjawalku, and X. J. Meng. "Epitope Mapping of the Major Capsid Protein of Type 2 Porcine Circovirus (PCV2) by Using Chimeric PCV1 and PCV2." Journal of Virology 78, no. 15 (August 1, 2004): 8135–45. http://dx.doi.org/10.1128/jvi.78.15.8135-8145.2004.
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ABSTRACT Type 2 porcine circovirus (PCV2) is associated with postweaning multisystemic wasting syndrome in pigs, whereas the genetically related type 1 PCV (PCV1) is nonpathogenic. In this study, seven monoclonal antibodies (MAbs) against PCV2-ORF2 capsid protein were generated, biologically characterized, and subsequently used to map the antigenic sites of PCV2 capsid protein by using infectious PCV DNA clones containing PCV1/PCV2-ORF2 chimeras. The PCV1/PCV2-ORF2 chimeras were constructed by serial deletions of PCV2-ORF2 and replacement with the corresponding sequences of the PCV1-ORF2. The reactivities of chimeric PCV1/PCV2 clones in transfected PK-15 cells with the seven MAbs were detected by an immunofluorescence assay (IFA). The chimera (r140) with a deletion of 47 amino acids at the N terminus of PCV2-ORF2 reacted strongly to all seven MAbs. Expanding the deletion of PCV2-ORF2 from residues 47 to 57 (r175) abolished the recognition of MAb 3B7, 3C11, 4A10, 6H2, or 8F6 to the chimera. Further deletion of PCV2-ORF2 to 62 residues disrupted the binding of this chimera to all seven MAbs. IFA reactivities with all MAbs were absent when residues 165 to 233 at the C terminus of PCV2-ORF2 was replaced with that of PCV1-ORF2. Extending the sequence of PCV2-ORF2 from residues 165 (r464) to 185 (r526), 200 (r588), or 224 (r652) restored the ability of the three chimeras to react with MAbs 3C11, 6H2, 9H7, and 12G3 but not with 8F6, 3B7, or 4A10. When the four amino acids at the C terminus of r588 were replaced with that of PCV2-ORF2, the resulting chimera (r588F) reacted with all seven MAbs. The results from this study suggest that these seven MAbs recognized at least five different but overlapping conformational epitopes within residues 47 to 63 and 165 to 200 and the last four amino acids at the C terminus of the PCV2 capsid protein.
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Hizanidis, Johanne, Vasileios G. Kanas, Anastasios Bezerianos, and Tassos Bountis. "Chimera States in Networks of Nonlocally Coupled Hindmarsh–Rose Neuron Models." International Journal of Bifurcation and Chaos 24, no. 03 (March 2014): 1450030. http://dx.doi.org/10.1142/s0218127414500308.
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We have identified the occurrence of chimera states for various coupling schemes in networks of two-dimensional and three-dimensional Hindmarsh–Rose oscillators, which represent realistic models of neuronal ensembles. This result, together with recent studies on multiple chimera states in nonlocally coupled FitzHugh–Nagumo oscillators, provide strong evidence that the phenomenon of chimeras may indeed be relevant in neuroscience applications. Moreover, our work verifies the existence of chimera states in coupled bistable elements, whereas to date chimeras were known to arise in models possessing a single stable limit cycle. Finally, we have identified an interesting class of mixed oscillatory states, in which desynchronized neurons are uniformly interspersed among the remaining ones that are either stationary or oscillate in synchronized motion.
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Monga, Luigi, and Sebastiano Vassalli. "La chimera." World Literature Today 65, no. 1 (1991): 97. http://dx.doi.org/10.2307/40146174.
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Waxman, Tobaron. "Chimera Project." TSQ: Transgender Studies Quarterly 9, no. 1 (February 1, 2022): 140–42. http://dx.doi.org/10.1215/23289252-9517364.
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Mulligan, M. S., S. R. Watson, C. Fennie, and P. A. Ward. "Protective effects of selectin chimeras in neutrophil-mediated lung injury." Journal of Immunology 151, no. 11 (December 1, 1993): 6410–17. http://dx.doi.org/10.4049/jimmunol.151.11.6410.
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Abstract Recombinant selectin chimeric molecules featuring the joining of the extracellular domains of L-, P-, and E-selectin to the CH2 and CH3 domains of human IgG1 have been evaluated for their ability to protect against neutrophil-dependent lung injury in rats after systemic activation of C caused by vascular infusion of cobra venom factor (CVF) or lung injury that follows intrapulmonary deposition of IgG immune complexes. Previous studies using anti-selectin antibodies have suggested that the former model is P-selectin dependent, whereas the latter is E-selectin dependent. Requirements for L-selectin have not been identified because of lack of reagents. For the current studies employing the CVF model of lung injury, infusion of P-selectin-Ig chimera reduced injury (as assessed by changes in permeability and hemorrhage) in a dose-dependent manner, with parallel reductions in lung myeloperoxidase (MPO) content. Similar results were obtained with the L-selectin-Ig chimera, whereas the E-selectin-Ig chimera was not protective and failed to alter MPO content. In contrast, in the IgG immune complex model of lung injury, the L- and E-selectin-Ig chimeras both showed dose-related protective effects and reductions in MPO content, whereas the P-selectin-Ig chimera failed to protect against injury and did not alter MPO content in this model of lung injury. In all cases of blocking of injury, this was incomplete, suggesting multi-selectin engagement or inadequate amounts of selectin-Ig chimeras employed. These data indicate that neutrophil recruitment and attendant lung injury in the CVF model are L- and P-selectin dependent and E-selectin-independent, whereas in the IgG immune complex model, neutrophil recruitment and lung injury are L- and E-selectin-dependent but independent of P-selectin. Thus, differing selectin requirements for acute inflammatory lung injury have been identified.
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LaFlamme, S. E., L. A. Thomas, S. S. Yamada, and K. M. Yamada. "Single subunit chimeric integrins as mimics and inhibitors of endogenous integrin functions in receptor localization, cell spreading and migration, and matrix assembly." Journal of Cell Biology 126, no. 5 (September 1, 1994): 1287–98. http://dx.doi.org/10.1083/jcb.126.5.1287.
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The ability of single subunit chimeric receptors containing various integrin beta intracellular domains to mimic and/or inhibit endogenous integrin function was examined. Chimeric receptors consisting of the extracellular and transmembrane domains of the small subunit of the human interleukin-2 receptor connected to either the beta 1, beta 3, beta 3B, or beta 5 intracellular domain were transiently expressed in normal human fibroblasts. When expressed at relatively low levels, the beta 3 and beta 5 chimeras mimicked endogenous ligand-occupied integrins and, like the beta 1 chimera (LaFlamme, S. E., S. K. Akiyama, and K. M. Yamada. 1992. J. Cell Biol. 117:437), concentrated with endogenous integrins in focal adhesions and sites of fibronectin fibril formation. In contrast, the chimeric receptor containing the beta 3B intracellular domain (a beta 3 intracellular domain modified by alternative splicing) was expressed diffusely on the cell surface, indicating that alternative splicing can regulate integrin receptor distribution by an intracellular mechanism. Furthermore, when expressed at higher levels, the beta 1 and beta 3 chimeric receptors functioned as dominant negative mutants and inhibited endogenous integrin function in localization to fibronectin fibrils, fibronectin matrix assembly, cell spreading, and cell migration. The beta 5 chimera was a less effective inhibitor, and the beta 3B chimera and the reporter lacking an intracellular domain did not inhibit endogenous integrin function. Comparison of the relative levels of expression of the transfected beta 1 chimera and the endogenous beta 1 subunit indicated that in 10 to 15 h assays, the beta 1 chimera can inhibit cell spreading when expressed at levels approximately equal to the endogenous beta 1 subunit. Levels of chimeric receptor expression that inhibited cell spreading also inhibited cell migration, whereas lower levels were able to inhibit alpha 5 beta 1 localization to fibrils and matrix assembly. Our results indicate that single subunit chimeric integrins can mimic and/or inhibit endogenous integrin receptor function, presumably by interacting with cytoplasmic components critical for endogenous integrin function. Our results also demonstrate that beta intracellular domains, expressed in this context, display specificity in their abilities to mimic and inhibit endogenous integrin function. Furthermore, the approach that we have used permits the analysis of intracellular domain function in the processes of cell spreading, migration and extracellular matrix assembly independent of effects due to the rest of integrin dimers. This approach should prove valuable in the further analysis of integrin intracellular domain function in these and other integrin-mediated processes requiring the interaction of integrins with cytoplasmic components.
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Myers, K. J., J. P. Dougherty, and Y. Ron. "In vivo antigen presentation by both brain parenchymal cells and hematopoietically derived cells during the induction of experimental autoimmune encephalomyelitis." Journal of Immunology 151, no. 4 (August 15, 1993): 2252–60. http://dx.doi.org/10.4049/jimmunol.151.4.2252.
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Abstract A fundamental issue in the etiology of autoimmune diseases of the central nervous system such as multiple sclerosis and its animal counterpart experimental autoimmune encephalomyelitis (EAE) concerns the identity of cells capable of presenting autoantigen to the T cells that mediate these diseases. The prevailing dogma is that only bone marrow-derived cells function as APC during EAE induction. We have addressed this issue by studying EAE induction in mouse bone marrow chimeras, and have found that although bone marrow-derived APC such as macrophages and brain microglial cells are more efficient at presenting autoantigen, brain parenchymal cells such as astrocytes and endothelial cells are also capable of inducing disease. EAE was induced in these chimeras by the adoptive transfer of encephalitogenic T cell lines designed to be MHC-histocompatible with APC contained either within the hematopoietic system of the chimera or with APC resident to the brain of the chimera. The subsequent development of EAE in these chimeras then indicated which population of cells served as in vivo APC during EAE pathogenesis. Possible effects of alloreactivity between the host chimera and the adoptively transferred T cells were eliminated by using encephalitogenic T cell lines made tolerant to the haplotype(s) of the recipient chimera.
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Kang, Hyojeung, Min Feng, Megan E. Schroeder, David P. Giedroc, and Julian L. Leibowitz. "Putative cis-Acting Stem-Loops in the 5′ Untranslated Region of the Severe Acute Respiratory Syndrome Coronavirus Can Substitute for Their Mouse Hepatitis Virus Counterparts." Journal of Virology 80, no. 21 (August 18, 2006): 10600–10614. http://dx.doi.org/10.1128/jvi.00455-06.
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ABSTRACT Consensus covariation-based secondary structural models for the 5′ 140 nucleotides of the 5′ untranslated regions (5′UTRs) from mouse hepatitis virus (MHV) and severe acute respiratory syndrome coronavirus (SCoV) were developed and predicted three major helical stem-loop structures, designated stem-loop 1 (SL1), SL2, and SL4. The SCoV 5′UTR was predicted to contain a fourth stem-loop, named SL3, in which the leader transcriptional regulatory sequence (TRS) is folded into a hairpin loop. cDNAs corresponding to MHV/SCoV chimeric genomes were constructed by replacing the complete MHV 5′UTR with the corresponding SCoV sequence and by separately replacing MHV 5′UTR putative SL1, putative SL2, TRS, and putative SL4 with the corresponding SCoV sequences. Chimeric genomes were transcribed in vitro, and viruses were recovered after electroporation into permissive cells. Genomes in which the MHV 5′UTR SL1, SL2, and SL4 were individually replaced by their SCoV counterparts were viable. Chimeras containing the complete SCoV 5′UTR or the predicted SCoV SL3 were not viable. A chimera containing the SCoV 5′UTR in which the SCoV TRS was replaced with the MHV TRS was also not viable. The chimera containing the entire SCoV 5′UTR failed to direct the synthesis of any virus-specific RNA. Replacing the SCoV TRS with the MHV TRS in the MHV/5′UTR SCoV chimera permitted the synthesis of minus-sense genome-sized RNA but did not support the production of positive- or minus-sense subgenomic RNA7. A similar phenotype was obtained with the MHV/SCoV SL3 chimera. These results suggest a role for the TRS in the replication of minus-sense genomic RNA in addition to its known function in subgenomic RNA synthesis.
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Koplin, Julian J., and Julian Savulescu. "Time to rethink the law on part-human chimeras." Journal of Law and the Biosciences 6, no. 1 (May 15, 2019): 37–50. http://dx.doi.org/10.1093/jlb/lsz005.
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Abstract It may soon be possible to generate human tissues and organs inside of part-human chimeras via a technique known as interspecies blastocyst complementation. Using Australian legislation as a case study, we show why this technique of creating part-human chimeras falls within the gaps of existing legislation. We give an overview of the key ethical issues raised by part-human chimera research, and we describe how well these issues are met by a range of possible regulatory approaches. We ultimately argue that regulation of part-human chimera research should be (re)designed to balance two key aims: to facilitate ethical research involving part-human chimeras and to prevent unethical experimentation with chimeras that have an uncertain—and potentially substantial—degree of moral status.
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Yang, Xia, and Peter N. Walsh. "An ordered sequential mechanism for Factor IX and Factor IXa binding to platelet receptors in the assembly of the Factor X-activating complex." Biochemical Journal 390, no. 1 (August 9, 2005): 157–67. http://dx.doi.org/10.1042/bj20050029.
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To define the contributions of the Ω-loop of the Gla (γ-carboxyglutamic acid) domain and the EGF2 (second epidermal growth factor) domain of FIXa (Factor IXa) in the assembly of the FX-activating complex on activated platelets and phospholipid membranes, three recombinant FIXa chimeras were prepared with corresponding residues from the homologous coagulation protein, FVII: (i) Gly4–Gln11 (FIXa7Ωloop), (ii) Cys88–Cys124 (FIXa7EGF2), and (iii) both Gly4–Gln11 and Cys88–Cys124 (FIXa7Ωloop7EGF2). All three chimeras were similar to wild-type FIXa, as assessed by SDS/PAGE, active-site titration, content of Gla residues, activation rates by FXIa and rates of FXa generation in solution. Titrations of FX or FVIIIa on SFLLRN peptide-activated platelets and on phospholipid vesicles in the presence of FVIIIa revealed normal substrate and cofactor binding to all chimeras. In kinetic assays in the presence of phospholipid vesicles and FVIIIa, compared with wild-type FIXa Kd, app∼4 nM, the FIX7Ωloop chimera showed a 1.6-fold increase in Kd, app, the FIX7EGF2 chimera had a 7.4-fold increase in Kd, app, and the FIX7Ωloop7EGF2 chimera showed a 21-fold increase in Kd, app. In kinetic assays and equilibrium platelet-binding assays with activated platelets and FVIIIa, compared with wild-type FIXa (Vmax∼5 nM min−1; Kd, app∼0.5 nM; Bmax∼550 sites/platelet; Kd∼0.5 nM), the FIX7Ωloop chimera displayed 2-fold decreases in Vmax and Bmax and 2-fold increases in Kd, app and Kd. The FIX7EGF2 chimera displayed 2-fold decreases in Vmax and Bmax and 10-fold increases in Kd, app and Kd. The FIX7Ωloop7EGF2 chimera showed non-saturable curves and severely impaired rates of FXa generation, and non-saturable, non-specific, low-level binding to activated platelets. Thus both the Gla domain Ω-loop (Gly4–Gln11) and the EGF2 domain (Cys88–Cys124) are required to mediate the normal assembly of the FX-activating complex on activated platelets and on phospholipid membranes.
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Kabiri, Mona, Mohsen Tafaghodi, Mohammad Reza Saberi, Maliheh Moghadam, Seyed Abdolrahim Rezaee, and Mojtaba Sankian. "Separation of the Epitopes in a Multi-Epitope Chimera: Helical or Flexible Linkers." Protein & Peptide Letters 27, no. 7 (August 13, 2020): 604–13. http://dx.doi.org/10.2174/0929866526666191112124602.
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Background: The engineered chimeric peptides including functional multi-epitope structures fused by various peptide linkers are widely applied in biotechnological research to improve the expression level and biological activity of chimera. Objective: The aim of our study was to evaluate the effect of helical and flexible linkers on solubility, expression level and folding of multi-epitope chimera containing four epitopes of Human T Lymphotropic Virus Type 1 (HTLV-1). Methods: For this purpose, the chimera sequences connected by the helical or flexible linker were inserted into different plasmid vectors and expressed in E. coli strains. The expressed products were analyzed using SDS-PAGE and Western blot techniques. Additionally, the molecular modeling study of the chimera with helical or flexible linker was performed using iterative threading assembly refinement (I-TASSER) to attain their three-dimensional structures. Results: Comparison of the chimera expression indicated that the insertion of a flexible (GGGGS)3 linker among chimera epitopes could significantly enhance the level of expression, whereas, the low-level of chimera expression was observed for chimera containing the contiguous helical (EAAAK)5 linker. According to the results of sequence alignment and plasmid stability test, the structure and function of a consecutive helical linker among chimera epitopes were similar to porins as the outer-membrane pore-forming proteins. The molecular modeling results confirmed our experimental study. Conclusion: This investigation illustrated the key role of linker design in determining the expression level of multi-epitope chimera and conformational folding.
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Gupta, Goutam, Abhaya Dandekar, Hossein Gouran, Cecilia Aguero, George Bruening, Paul A. Feldstein, Rafael Nascimento, et al. "Pathogen clearance by engineering novel host innate immunity (P1251)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 56.8. http://dx.doi.org/10.4049/jimmunol.190.supp.56.8.
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Abstract A few years ago, we introduced a concept that a protein chimera of pathogen recognition and lysis domains would be able to rapidly clear a broad-spectrum of pathogens [Crit Rev Immunol 2007;27(3):233-245]. For a wide variety of viral, bacterial, and fungal pathogens, appropriate recognition and lysis domains can be chosen from the host innate immune repertoire. A chimera of the recognition and lysis domains would be designed with the aid of a flexible linker to ensure synergy of the two functions and therefore, the rapid clearance of the targeted pathogen. In this work, we demonstrate the design of such a chimera and the efficacy of this chimera in clearing a plant pathogen Xylella fastidiosa (Xf) that causes diseases in multiple plants of economic importance. The most notable ones are Pierce’s disease (PD) in grape and variegated chlorosis (CVC) in citrus. Specifically, we show the construction of the transgenic grapevines expressing a protein chimera of recognition and lysis domains specific for Xf. This chimera clears Xf from the xylem (the site of colonization) and blocks the development of PD [Proc Natl Acad Sci U S A. 2012;109(10):3721-3725]. The same chimera can be applied to block CVC. Finally, we indicate how such chimeras of recognition and lysis domains can be developed to target multiple human pathogens.
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Gross, Mor, Nathalie Ben-Califa, Hans Carl Hasselbalch, Mary Frances McMullin, Melanie Percy, Celeste Bento, Holger Cario, Milen Minkov, and Drorit Neumann. "Polycythemia-Inducing Mutations In The Erythropoietin Receptor (EPOR): Mechanism and Function Elucidated By EGFR– EPOR Chimeras." Blood 122, no. 21 (November 15, 2013): 2174. http://dx.doi.org/10.1182/blood.v122.21.2174.2174.
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Abstract Absolute erythrocytosis are rare disorders characterized by a significant increase of the red blood cell mass which is reflected by an increased number of circulating erythrocytes, high hematocrit and hemoglobin. Primary familial and congenital polycythemia (PFCP, familial erythrocytosis type 1, OMIM #133100) is an inherited form of this disease, caused by erythropoietin (EPO) hypersensitivity of erythroid precursor cells. A number of mutations in the intracellular region of the EPO receptor (EPOR) have been found in recent years to be associated with manifestation of the disease. The objective of the study was to explore the mechanisms by which these mutations in the cytosolic domain of EPOR may induce the erythrocytosis phenotype. The research strategy was to construct chimeric receptors that contain the extracellular and transmembrane regions of the human epidermal growth factor receptor (EGFR) fused to the cytosolic domain of the human EPOR. The moiety of the EPOR intracellular region was mutated according to 4 novel mutations discovered in the cytosolic domain of the EPOR in PFCP patients. This design enabled EPOR signaling to be triggered by EGF binding to the extracellular domain of the chimera. The working hypothesis was that since the cytosolic, EPOR region of the chimera was generated based on mutations discovered in PFCP patients, any differences in the chimera-related effects would be specifically attributed to the mutations. The experiments were performed in an in vitro system, in which the Wild-Type (WT) EGFR– EPOR and the EGFR– EPOR chimeras bearing the mutated EPOR cytosolic domain were stably transfected into the EPO-dependent human erythroleukemia cell-line UT7. As these cells lack the EGF receptor, the natural EPOR signaling can be avoided when the transfected cells are grown with, or activated by, EGF. Using this system we have analyzed 4 novel EPOR mutations discovered in PFCP patients: 2 deletions which lead to frameshifts, premature stop codons and truncations (Del1387-1390 and Del1378-1412), a nonsense mutation (C1371A) which results in truncation of the receptor, and a missense mutation (G1445A) which results in the substitution of arginine 437 to histidine. A panel of experiments was performed on UT7 cells expressing the WT EGFR-EPOR chimera or EGFR– EPOR chimeras bearing the EPOR cytosolic PFCP-associated mutations. We addressed the degradation rates of the chimeric receptors, the kinetics of EGF induced STAT5 and MAPK/ERK signaling cascades and the levels of glycan-maturation and cell-surface expression of the chimeras. Cell viability analysis revealed that UT7 cells expressing either one of the 4 mutated chimeric receptors proliferated even under very low (0.01 ng/ml) EGF concentrations, as opposed to cells expressing the WT chimera, which did not proliferate under these conditions. UT7 cells expressing the mutated chimeras also displayed enhanced growth, which may indicate that indeed the mutations are the underlying cause of PFCP. Notably, our findings are the first description of a missense EPOR mutation that is associated with over-activity of the EPOR and with development of a polycythemic phenotype. Furthermore, we found that each of the 4 EPOR mutations differentially affected signaling and metabolism of the chimeric receptors. Hence, (i) Del1387-1390, showed higher levels of glycan-mature protein, as well as slower degradation rates, and conferred slower attenuation of EGF-induced pSTAT5. (ii) Del1378-1412 exhibited slower degradation rates and higher levels of glycan-mature protein. (iii) The nonsense mutation, C1371A, displayed higher cell surface levels, slower degradation rates and relayed constitutive activation of STAT5. (iv) The missense mutation, G1445A, mediated a slower attenuation of EGF induced MAPK/ERK signaling. Our study supports the evidence regarding the role of the cytosolic region of EPOR in metabolism of the receptor and sheds new light on the mechanisms underlying erythrocytosis-inducing mutations in the EPOR. HH, MFMcM, MJP, CB, HC and DN are members MPN&MPNr-EuroNet (COST Action BM0902) Disclosures: No relevant conflicts of interest to declare.
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Sensini, Francesca Irene. "Utopia con chimera." Italies, no. 24 (December 18, 2020): 217–32. http://dx.doi.org/10.4000/italies.8484.
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Hallock, Geoffrey G. "The Chimera Flap." Annals of Plastic Surgery 78, no. 2 (February 2017): 223–29. http://dx.doi.org/10.1097/sap.0000000000000884.
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Tom, Erica. "My Own Chimera." WSQ: Women's Studies Quarterly 44, no. 1-2 (2016): 304–5. http://dx.doi.org/10.1353/wsq.2016.0022.
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