Journal articles: 'RIP-1'

1

WEI, YI-HUAN. "SYMMETRIES ABOUT BIG RIP IN SO(1, 1) PHANTOM UNIVERSE." Modern Physics Letters A 21, no. 37 (December 7, 2006): 2845–52. http://dx.doi.org/10.1142/s0217732306020299.

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We study the SO(1, 1) dark energy model with the inverse power law potential, V = V0Φ-n, and find for n<2 the model has the late-time phantom property and the universe will evolve to the future Big Rip. The inverse linear potential is a special case, for which the field and the scalar factor are respectively T-invariant and CT-invariant about the Big Rip.

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CHEN, YONG P., Z. H. WANG, R. M. LEWIS, P. D. YE, L. W. ENGEL, D. C. TSUI, L. N. PFEIFFER, and K. W. WEST. "AC MAGNETOTRANSPORT IN REENTRANT INSULATING PHASES OF TWO-DIMENSIONAL ELECTRONS NEAR 1/5 AND 1/3 LANDAU FILLINGS." International Journal of Modern Physics B 18, no. 27n29 (November 30, 2004): 3553–56. http://dx.doi.org/10.1142/s0217979204027001.

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We have measured high frequency magnetotransport of a high quality two-dimensional electron system (2DES) near the reentrant insulating phase (RIP) at Landau fillings (ν) between 1/5 and 2/9. The magnetoconductivity in the RIP has resonant behavior around 150 MHz, showing a peak at ν~0.21. Our data support the interpretation of the RIP as due to some pinned electron solid. We have also investigated a narrowly confined 2DES recently found to have a RIP at 1/3<ν<1/2 and we have revealed features, not seen in DC transport, that suggest some intriguing interplay between the 1/3 FQHE and RIP.

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Cusson, Nicole, Sarah Oikemus, Elizabeth D. Kilpatrick, Leslie Cunningham, and Michelle Kelliher. "The Death Domain Kinase RIP Protects Thymocytes from Tumor Necrosis Factor Receptor Type 2–induced Cell Death." Journal of Experimental Medicine 196, no. 1 (July 1, 2002): 15–26. http://dx.doi.org/10.1084/jem.20011470.

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Fas and the tumor necrosis factor receptor (TNFR)1 regulate the programmed cell death of lymphocytes. The death domain kinase, receptor interacting protein (rip), is recruited to the TNFR1 upon receptor activation. In vitro, rip−/− fibroblasts are sensitive to TNF-induced cell death due to an impaired nuclear factor κB response. Because rip−/− mice die at birth, we were unable to examine the effects of a targeted rip mutation on lymphocyte survival. To address the contribution of RIP to immune homeostasis, we examined lethally irradiated mice reconstituted with rip−/− hematopoietic precursors. We observed a decrease in rip−/− thymocytes and T cells in both wild-type C57BL/6 and recombination activating gene 1−/− irradiated hosts. In contrast, the B cell and myeloid lineages are unaffected by the absence of rip. Thus, the death domain kinase rip is required for T cell development. Unlike Fas-associated death domain, rip does not regulate T cell proliferation, as rip−/− T cells respond to polyclonal activators. However, rip-deficient mice contain few viable CD4+ and CD8+ thymocytes, and rip−/− thymocytes are sensitive to TNF-induced cell death. Surprisingly, the rip-associated thymocyte apoptosis was not rescued by the absence of TNFR1, but appears to be rescued by an absence of TNFR2. Taken together, this study implicates RIP and TNFR2 in thymocyte survival.

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Sackner, M. A., H. Watson, A. S. Belsito, D. Feinerman, M. Suarez, G. Gonzalez, F. Bizousky, and B. Krieger. "Calibration of respiratory inductive plethysmograph during natural breathing." Journal of Applied Physiology 66, no. 1 (January 1, 1989): 410–20. http://dx.doi.org/10.1152/jappl.1989.66.1.410.

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We describe a single-posture method for deriving the proportionality constant (K) between rib cage (RC) and abdominal (AB) amplifiers of the respiratory inductive plethysmograph (RIP). Qualitative diagnostic calibration (QDC) is based on equations of the isovolume maneuver calibration (ISOCAL) and is carried out during a 5-min period of natural breathing without using mouthpiece or mask. In this situation, K approximates the ratio of standard deviations (SD) of the uncalibrated changes of AB-to-RC volume deflections. Validity of calibration was evaluated by 1) analyzing RIP waveforms during an isovolume maneuver and 2) comparing changes of tidal volume (VT) amplitude and functional residual capacity (FRC) level measured by spirometry (SP) with RIP values. Comparisons of VT(RIP) to VT(SP) were also obtained in a variety of postures during natural (uninstructed) preferential RC and AB breathing and with voluntary changes of VT amplitude and FRC level. VT(RIP)-to-VT(SP) comparisons were equal to or closer than published reports for single posture, ISOCAL, multiple- and linear-regression procedures. QDC of RIP in supine posture with comparisons to SP in that posture and others showed better accuracy in horizontal than upright postures.

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Wang, Jin, Lei Wang, and Yu Kou. "The different roles of relative ingroup prototypicality in the outgroup attitudes of majority and minority groups." Group Processes & Intergroup Relations 21, no. 2 (August 29, 2016): 319–35. http://dx.doi.org/10.1177/1368430216663020.

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Based on the argument that the ingroup projection model may not be applicable to the minority group when addressing the effect of relative ingroup prototypicality (RIP) on outgroup attitudes, two studies investigated whether RIP and its effects on outgroup attitudes differ for the majority (Han) and an ethnic minority group (Tibetan). We measured RIP and outgroup attitudes in Study 1 ( N = 164) and manipulated RIP in Study 2 ( N = 145). The results indicated that the Hans presented high RIP, whereas the Tibetans presented low RIP. The effects of RIP on outgroup attitudes were moderated by group size: High RIP among Hans resulted in negative outgroup attitudes, whereas high RIP among Tibetans led to positive outgroup attitudes. These findings imply that improving the minority group’s RIP by making its culture prototypicality equal to that of the majority group would lead to positive outgroup attitudes.

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Moulton, Melissa, Gregory Dusek, Steve Elgar, and Britt Raubenheimer. "Comparison of Rip Current Hazard Likelihood Forecasts with Observed Rip Current Speeds." Weather and Forecasting 32, no. 4 (August 1, 2017): 1659–66. http://dx.doi.org/10.1175/waf-d-17-0076.1.

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Abstract Although rip currents are a major hazard for beachgoers, the relationship between the danger to swimmers and the physical properties of rip current circulation is not well understood. Here, the relationship between statistical model estimates of hazardous rip current likelihood and in situ velocity observations is assessed. The statistical model is part of a forecasting system that is being made operational by the National Weather Service to predict rip current hazard likelihood as a function of wave conditions and water level. The temporal variability of rip current speeds (offshore-directed currents) observed on an energetic sandy beach is correlated with the hindcasted hazard likelihood for a wide range of conditions. High likelihoods and rip current speeds occurred for low water levels, nearly shore-normal wave angles, and moderate or larger wave heights. The relationship between modeled hazard likelihood and the frequency with which rip current speeds exceeded a threshold was assessed for a range of threshold speeds. The frequency of occurrence of high (threshold exceeding) rip current speeds is consistent with the modeled probability of hazard, with a maximum Brier skill score of 0.65 for a threshold speed of 0.23 m s−1, and skill scores greater than 0.60 for threshold speeds between 0.15 and 0.30 m s−1. The results suggest that rip current speed may be an effective proxy for hazard level and that speeds greater than ~0.2 m s−1 may be hazardous to swimmers.

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Yu, Xiaoliang, Yun Li, Qin Chen, Chenhe Su, Zili Zhang, Chengkui Yang, Zhilin Hu, et al. "Herpes Simplex Virus 1 (HSV-1) and HSV-2 Mediate Species-Specific Modulations of Programmed Necrosis through the Viral Ribonucleotide Reductase Large Subunit R1." Journal of Virology 90, no. 2 (November 11, 2015): 1088–95. http://dx.doi.org/10.1128/jvi.02446-15.

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ABSTRACTReceptor-interacting protein kinase 3 (RIP3) and its substrate mixed-lineage kinase domain-like protein (MLKL) are core regulators of programmed necrosis. The elimination of pathogen-infected cells by programmed necrosis acts as an important host defense mechanism. Here, we report that human herpes simplex virus 1 (HSV-1) and HSV-2 had opposite impacts on programmed necrosis in human cells versus their impacts in mouse cells. Similar to HSV-1, HSV-2 infection triggered programmed necrosis in mouse cells. However, neither HSV-1 nor HSV-2 infection was able to induce programmed necrosis in human cells. Moreover, HSV-1 or HSV-2 infection in human cells blocked tumor necrosis factor (TNF)-induced necrosis by preventing the induction of an RIP1/RIP3 necrosome. The HSV ribonucleotide reductase large subunit R1 was sufficient to suppress TNF-induced necrosis, and its RIP homotypic interaction motif (RHIM) domain was required to disrupt the RIP1/RIP3 complex in human cells. Therefore, this study provides evidence that HSV has likely evolved strategies to evade the host defense mechanism of programmed necrosis in human cells.IMPORTANCEThis study demonstrated that infection with HSV-1 and HSV-2 blocked TNF-induced necrosis in human cells while these viruses directly activated programmed necrosis in mouse cells. Expression of HSV R1 suppressed TNF-induced necrosis of human cells. The RHIM domain of R1 was essential for its association with human RIP3 and RIP1, leading to disruption of the RIP1/RIP3 complex. This study provides new insights into the species-specific modulation of programmed necrosis by HSV.

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8

Munz, Barbara, Eberhard Hildt, Matthew L. Springer, and Helen M. Blau. "RIP2, a Checkpoint in Myogenic Differentiation." Molecular and Cellular Biology 22, no. 16 (August 15, 2002): 5879–86. http://dx.doi.org/10.1128/mcb.22.16.5879-5886.2002.

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ABSTRACT Using a subtractive cDNA library hybridization approach, we found that receptor interacting protein 2 (RIP2), a tumor necrosis factor receptor 1 (TNFR-1)-associated factor, is a novel early-acting gene that decreases markedly in expression during myogenic differentiation. RIP2 consists of three domains: an amino-terminal kinase domain, an intermediate domain, and a carboxy-terminal caspase activation and recruitment domain (CARD). In some cell types, RIP2 has been shown to be a potent inducer of apoptosis and an activator of NF-κB. To analyze the function of RIP2 during differentiation, we transduced C2C12 myoblasts with retroviral vectors to constitutively produce RIP2 at high levels. When cultured in growth medium, these cells did not show an enhanced rate of proliferation compared to controls. When switched to differentiation medium, however, they continued to proliferate, whereas control cells withdrew from the cell cycle, showed increased expression of differentiation markers such as myogenin, and began to differentiate into multinucleated myotubes. The complete RIP2 protein appeared to be necessary to inhibit myogenic differentiation, since two different deletion mutants lacking either the amino-terminal kinase domain or the carboxy-terminal CARD had no effect. A mutant deficient in kinase activity, however, had effects similar to wild-type RIP2, indicating that phosphorylation was not essential to the function of RIP2. Furthermore, RIP proteins appeared to be important during myogenic differentiation in vivo, as we detected a marked decrease in expression of the RIP2 homolog RIP in several muscle tissues of the dystrophic mdx mouse, a model for continuous muscle degeneration and regeneration. We conclude that RIP proteins can act independently of TNFR-1 stimulation by ligand to modulate downstream signaling pathways, such as activation of NF-κB. These results implicate RIP2 in a previously unrecognized role: a checkpoint for myogenic proliferation and differentiation.

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Jeong, Mi-Young, Dae-Hee Park, Min-Cheol Kim, Jinbong Park, Dae-Seung Kim, Yong-Deok Jeon, Su-Jin Kim, et al. "Saengmaeksaninhibits inflammatory mediators by suppressing RIP-2/caspase-1 activation." Immunopharmacology and Immunotoxicology 35, no. 2 (January 28, 2013): 241–50. http://dx.doi.org/10.3109/08923973.2012.757617.

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10

Huang, Chuanjiang, Yinan Luo, Jingwei Zhao, Fuwei Yang, Hongwei Zhao, Wenhai Fan, and Pengfei Ge. "Shikonin Kills Glioma Cells through Necroptosis Mediated by RIP-1." PLoS ONE 8, no. 6 (June 28, 2013): e66326. http://dx.doi.org/10.1371/journal.pone.0066326.

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11

Sandoval, Rafael, Robert D. Boyd, Alena N. Kiszter, Yeva Mirzakhanyan, Paola Santibańez, Paul D. Gershon, and Michael L. Hayes. "Stable native RIP 9 complexes associate with C‐to‐U RNA editing activity, PPR s, RIP s, OZ 1, ORRM 1 and ISE 2." Plant Journal 99, no. 6 (June 26, 2019): 1116–26. http://dx.doi.org/10.1111/tpj.14384.

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12

Bhat, Ashwin, Felicite K. Noubissi, Meenal Vyas, and Durgadas P. Kasbekar. "Genetic Analysis of Wild-Isolated Neurospora crassa Strains Identified as Dominant Suppressors of Repeat-Induced Point Mutation." Genetics 164, no. 3 (July 1, 2003): 947–61. http://dx.doi.org/10.1093/genetics/164.3.947.

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Abstract Repeat-induced point mutation (RIP) in Neurospora results in inactivation of duplicated DNA sequences. RIP is thought to provide protection against foreign elements such as retrotransposons, only one of which has been found in N. crassa. To examine the role of RIP in nature, we have examined seven N. crassa strains, identified among 446 wild isolates scored for dominant suppression of RIP. The test system involved a small duplication that targets RIP to the easily scorable gene erg-3. We previously showed that RIP in a small duplication is suppressed if another, larger duplication is present in the cross, as expected if the large duplication competes for the RIP machinery. In two of the strains, RIP suppression was associated with a barren phenotype—a characteristic of Neurospora duplications that is thought to result in part from a gene-silencing process called meiotic silencing by unpaired DNA (MSUD). A suppressor of MSUD (Sad-1) was shown not to prevent known large duplications from impairing RIP. Single-gene duplications also can be barren but are too short to suppress RIP. RIP suppression in strains that were not barren showed inheritance that was either simple Mendelian or complex. Adding copies of the LINE-like retrotransposon Tad did not affect RIP efficiency.

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VAN DAMME, Els J. M., Annick BARRE, Luigi BARBIERI, Paola VALBONESI, Pierre ROUGE, Fred VAN LEUVEN, Fiorenzo STIRPE, and Willy J. PEUMANS. "Type 1 ribosome-inactivating proteins are the most abundant proteins in iris (Iris hollandica var. Professor Blaauw) bulbs: characterization and molecular cloning." Biochemical Journal 324, no. 3 (June 15, 1997): 963–70. http://dx.doi.org/10.1042/bj3240963.

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The most abundant protein of Iris bulbs has been identified as a type 1 ribosome-inactivating protein (RIP). Analysis of the purified proteins and molecular cloning of the corresponding cDNAs demonstrated that this type 1 RIP is a mixture of three isoforms that exhibit a high degree of sequence identity and have similar, though not identical, ribosome-inactivating and polynucleotide:adenosine glycosidase activities. The accumulation of large quantities of type 1 RIP in a vegetative storage organ suggests that this presumed defence-related protein also plays a role in the nitrogen-storage metabolism of the bulb.

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Revow, M. D., S. J. England, H. A. Stogryn, and D. L. Wilkes. "Comparison of calibration methods for respiratory inductive plethysmography in infants." Journal of Applied Physiology 63, no. 5 (November 1, 1987): 1853–61. http://dx.doi.org/10.1152/jappl.1987.63.5.1853.

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In infants under the age of 6 mo respiratory inductive plethysmograph (RIP)-calculated tidal volumes (VT) were compared with simultaneously measured volumes using a pneumotachograph (PNT) to 1) assess whether using multiple points (MP) along the inspiratory profile of a breath is superior to using only VT when calculating volume-motion (VM) coefficients, 2) verify the assumption of independent contributions of the abdomen and rib cage to VT, which was accomplished by extending the normal RIP model to include a term representing interaction between these two compartments, and 3) investigate whether VM coefficients are sleep-state dependent. Neither use of multiple points nor inclusion of the interacting term improved the performance of the RIP over that observed using a simple two-compartment model with VT measurements. However, VM coefficients obtained during quiet sleep (QS) were not reliable when used during rapid-eye-movement (REM) sleep, suggesting that coefficients obtained during one sleep state may not be applicable to another state where there is a substantial change in the relative abdominal/rib cage contributions to VT.

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15

Rawson, Robert B. "Regulated intramembrane proteolysis: from the endoplasmic reticulum to the nucleus." Essays in Biochemistry 38 (October 1, 2002): 155–68. http://dx.doi.org/10.1042/bse0380155.

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Regulated intramembrane proteolysis (Rip) is an ancient and widespread process by which cells transmit information from one compartment (the endoplasmic reticulum) to another (the nucleus). Two separate cleavages that are carried out by two separate proteases are required for Rip. The first protease cleaves its protein substrate within an extracytoplasmic domain; the second cleaves it within a membrane-spanning domain, releasing a functionally active fragment of the target protein. In eukaryotes, examples of Rip can be divided into two classes, according to the proteases that are involved and the orientation of the substrates with the membrane. Class 1 Rip involves type 1 transmembrane proteins and requires presenilin for cleavage within a membrane-spanning domain. In Class 2 Rip, the highly hydrophobic metalloprotease, site-2 protease, is required for cleavage within a membrane-spanning domain and substrates are type 2 transmembrane proteins. Both classes of Rip are implicated in diseases that are important in modern societies, such as hyperlipidaemias (via the sterol regulatory element binding protein pathway) and Alzheimer's disease (via processing of the amyloid precursor protein.)

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Butz, Anh T., Michel El Alam, William P. Irvin Jr., and Dale W. Stovall. "The Rothman Index: Assessing risk for 30-day readmission in gynecologic oncology service patients." Journal of Hospital Administration 8, no. 2 (April 10, 2019): 54. http://dx.doi.org/10.5430/jha.v8n2p54.

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Background: The Rothman Index (RI) is a previously validated, continuously computed score derived from 26 clinical measures that assesses a patient's clinical status. It has been used as a prognostic indicator in the intensive care setting and has been incorporated into the electronic medical record. This study was designed to determine its utility in assessing 30-day readmission rates in postoperative gynecologic oncology service patients. Methods: In this retrospective case-control study, gynecologic oncology service surgical patients readmitted within 30 days of discharge (cases) were matched 1:2 by procedure, diagnosis, age and comorbidities to non-readmitted gynecologic oncology surgical patients (controls). All procedures were performed at one center by a single surgeon. Rothman Index values were obtained immediately postoperative (RIp) and before discharge (RId), and the difference between these values was calculated (RIc). Rothman Index scores were compared between cases and controls. Results: In total, 24 cases were matched to 48 controls. The mean age of all study participants was 56 years. The RId was significantly different between groups, with median RId of 70 for readmitted subjects and 75.5 for controls (P = .029). Binomial regression of readmission on RI revealed an RId of 58.9 or less was associated with at least 50% likelihood of readmission (P = .017). Cases and controls did not significantly differ based on RIp or RIc, and were similar with respect to risk factors including diabetes, smoking, and BMI. Conclusion: Delaying discharge for patients with RI below a designated threshold may reduce gynecologic oncology postoperative readmission rates.

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Demidov, A. N., M. A. Karimbekov, and A. Yu Marchenkov. "Heating and Cooling Impact on Mechanical Properties of RIP Electric Insulator for High Voltage Inputs." Solid State Phenomena 265 (September 2017): 496–500. http://dx.doi.org/10.4028/www.scientific.net/ssp.265.496.

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The mechanical properties investigation results obtained by tension and indentation tests of RIP (resin impregnated paper) electric insulator are presented. Tension and indentation tests of the RIP electric insulation material in wide temperature range are conducted. The common relations between strength and temperature as well as between hardness and temperature for the RIP electric insulation are established. The ratio of ultimate tensile strength to Brinell hardness is performed to be constant (about 1/3) irrespective of temperature, that means a possibility of the RIP electric insulation mechanical properties evaluation by the instrumented indentation test.

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D’Amico, Eugenio, Hongxiang Hui, Nasif Khoury, Umberto Di Mario, and Riccardo Perfetti. "Pancreatic β-cells expressing GLP-1 are resistant to the toxic effects of immunosuppressive drugs." Journal of Molecular Endocrinology 34, no. 2 (April 2005): 377–90. http://dx.doi.org/10.1677/jme.1.01655.

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Glucose intolerance is often observed after pancreatic islet cell transplantation. The administration of immunosuppressive agents (ISD), necessary to avoid tissue rejection, is in part responsible for hyperglycemia. To investigate whether mouse insulinoma (MIN6) cells transfected with the glucagon like peptide-1 (GLP-1) fragment of the proglucagon gene (RIP/GLP-1 MIN6 cells) are resistant to the toxicity derived from the administration of ISD. RIP/GLP-1 MIN6 cells, as well as parental MIN6 cells, were exposed to a cocktail of ISD. The secretion of insulin and the expression of apoptosis-related proteins were investigated by RIA and western blot analysis. Cell apoptosis was quantified by FACS analysis. Finally, to study whether the antiapoptotic action of GLP-1 was a function of its effect on insulin secretion, or rather it was a direct effect of GLP-1, cells were cultured with or without diazoxide or exendin-9. GLP-1 improved the functional activity and the viability of cells exposed to ISD. The insulin secretion of RIP/GLP-1 MIN6 cells after exposure to ISD was preserved. The expression of GLP-1 by β-cells reduced the number of apoptotic cells and increased the expression of the antiapoptotic protein Bcl-2. GLP-1 also decreased the abundance of the proapoptotic markers PARP-p85 and Smac/Diablo. Treatment of cells with the diazoxide did not abolish the protective advantage that cells transfected with GLP-1 had; conversely the exposure of cells to exendin-9 was associated with a restored susceptibility to apoptosis. This report demonstrates that GLP-1 is capable of preserving β-cell function and protecting cells from apoptotic cell death.

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Prince, Heather, Ruanbao Zhou, and Lee Kroos. "Substrate Requirements for Regulated Intramembrane Proteolysis of Bacillus subtilis Pro-σK." Journal of Bacteriology 187, no. 3 (February 1, 2005): 961–71. http://dx.doi.org/10.1128/jb.187.3.961-971.2005.

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ABSTRACT During sporulation of Bacillus subtilis, pro-σK is activated by regulated intramembrane proteolysis (RIP) in response to a signal from the forespore. RIP of pro-σK removes its prosequence (amino acids 1 to 20), releasing σK from the outer forespore membrane into the mother cell cytoplasm, in a reaction catalyzed by SpoIVFB, a metalloprotease in the S2P family of intramembrane-cleaving proteases. The requirements for pro-σK to serve as a substrate for RIP were investigated by producing C-terminally truncated pro-σK fused at different points to the green fluorescent protein (GFP) or hexahistidine in sporulating B. subtilis or in Escherichia coli engineered to coexpress SpoIVFB. Nearly half of pro-σK (amino acids 1 to 117), including part of sigma factor region 2.4, was required for RIP of pro-σK-GFP chimeras in sporulating B. subtilis. Likewise, pro-σK-hexahistidine chimeras demonstrated that the N-terminal 117 amino acids of pro-σK are sufficient for RIP, although the N-terminal 126 amino acids, which includes all of region 2.4, allowed much better accumulation of the chimeric protein in sporulating B. subtilis and more efficient processing by SpoIVFB in E. coli. In contrast to the requirements for RIP, a much smaller N-terminal segment (amino acids 1 to 27) was sufficient for membrane localization of a pro-σK-GFP chimera. Addition or deletion of five amino acids near the N terminus allowed accurate processing of pro-σK, ruling out a mechanism in which SpoIVFB measures the distance from the N terminus to the cleavage site. A charge reversal at position 13 (substituting glutamate for lysine) reduced accumulation of pro-σK and prevented detectable RIP by SpoIVFB. These results elucidate substrate requirements for RIP of pro-σK by SpoIVFB and may have implications for substrate recognition by other S2P family members.

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Ghosh, T., Y. Vashi, K. Barman, and L. I. Singha. "Novel Ribosome-inactivating Protein (RIP) Isolated from Trichosanthes dioica Induces Apoptosis in HeLa Cell Line." International Journal of Bio-resource and Stress Management 12, no. 3 (June 30, 2021): 165–69. http://dx.doi.org/10.23910/1.2021.2221.

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Ribosome-inactivating proteins (RIPs) are toxic N-glycosidases that depurinate eukaryotic and prokaryotic rRNAs and thus interrupt protein synthesis during translation. In the present study, a protein of around 32 kDa, supposedly a RIP isolated from Trichosanthes dioica, was assessed for its potential to induce apoptosis in HeLa cells. Cell viability assay was done to measure cell proliferation and survivability. It was observed that cells viability decreased with the increase of decrease in dilution, i.e. when the sample was an undiluted one, the viability decreased drastically and almost came to less than 10%. To further check whether the isolated RIP could induce apoptosis, HeLa cells were treated with the test RIP. Immunoblotting was carried out using PARP poly (ADP-ribose) polymerase (PARP-1), a 113 kDa nuclear enzyme, which is considered a hallmark of cells undergoing apoptosis. HeLa cells were further analyzed for loss of mitochondrial membrane potential with JC-1 dye, which is an early event during apoptosis. Increased PARP breakdown in the RIP treated cells indicates that cells undergoing apoptosis and progressive loss of red J-aggregate fluorescence indicate that the isolated RIP from Trichosanthes dioica induces apoptosis in HeLa cells. The ability of apoptosis induction is comparable to another known RIP from Momordica charantia, which was used as a positive control. Promising results from the present study warrants the isolated RIP to be further explored for anticancer activities.

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Ye, Jin. "Transcription factors activated through RIP (regulated intramembrane proteolysis) and RAT (regulated alternative translocation)." Journal of Biological Chemistry 295, no. 30 (June 2, 2020): 10271–80. http://dx.doi.org/10.1074/jbc.rev120.012669.

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Transmembrane proteins are membrane-anchored proteins whose topologies are important for their functions. These properties enable regulation of certain transmembrane proteins by regulated intramembrane proteolysis (RIP) and regulated alternative translocation (RAT). RIP enables a protein fragment of a transmembrane precursor to function at a new location, and RAT leads to an inverted topology of a transmembrane protein by altering the direction of its translocation across membranes during translation. RIP mediated by site-1 protease (S1P) and site-2 protease (S2P) is involved in proteolytic activation of membrane-bound transcription factors. In resting cells, these transcription factors remain in the endoplasmic reticulum (ER) as inactive transmembrane precursors. Upon stimulation by signals within the ER, they are translocated from the ER to the Golgi. There, they are cleaved first by S1P and then by S2P, liberating their N-terminal domains from membranes and enabling them to activate genes in the nucleus. This signaling pathway regulates lipid metabolism, unfolded protein responses, secretion of extracellular matrix proteins, and cell proliferation. Remarkably, ceramide-induced RIP of cAMP response element–binding protein 3–like 1 (CREB3L1) also involves RAT. In resting cells, RIP of CREB3L1 is blocked by transmembrane 4 L6 family member 20 (TM4SF20). Ceramide inverts the orientation of newly synthesized TM4SF20 in membranes through RAT, converting TM4SF20 from an inhibitor to an activator of RIP of CREB3L1. Here, I review recent insights into RIP of membrane-bound transcription factors, focusing on CREB3L1 activation through both RIP and RAT, and discuss current open questions about these two signaling pathways.

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Radhitya, Made Leo, and Agus Harjoko. "Sistem Informasi Geografis Risiko Kemunculan Rip Current Menggunakan Decision Tree C4.5." IJCCS (Indonesian Journal of Computing and Cybernetics Systems) 10, no. 2 (July 31, 2016): 195. http://dx.doi.org/10.22146/ijccs.15949.

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One of the dangers that occur at the beach is rip current. Rip current poses significant danger for beachgoers. This paper proposes a method to predict the rip current's occurence risk by using decision tree generated using C4.5 algorithm. The output from the decision tree is rip current's occurrence risk. The case study for this research is the beach located at Rote Island, Rote Ndao, Nusa Tenggara Timur. Evaluation result shows that the accuracy is 0.84, and the precision is 0.61. The average recall value is 0.68 and the average F-measure is 0.59 in the range 0 to 1.

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23

Zelic, Matija, Justine E. Roderick, Joanne A. O’Donnell, Jesse Lehman, Sung Eun Lim, Harish P. Janardhan, Chinmay M. Trivedi, Manolis Pasparakis, and Michelle A. Kelliher. "RIP kinase 1–dependent endothelial necroptosis underlies systemic inflammatory response syndrome." Journal of Clinical Investigation 128, no. 5 (April 16, 2018): 2064–75. http://dx.doi.org/10.1172/jci96147.

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Habib, Robert H., Kee H. Pyon, Sherry E. Courtney, and Zubair H. Aghai. "Spectral characteristics of airway opening and chest wall tidal flows in spontaneously breathing preterm infants." Journal of Applied Physiology 94, no. 5 (May 1, 2003): 1933–40. http://dx.doi.org/10.1152/japplphysiol.00927.2002.

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We compared the harmonic content of tidal flows measured simultaneously at the mouth and chest wall in spontaneously breathing very low birth weight infants ( n = 16, 1,114 ± 230 g, gestation age: 28 ± 2 wk). Airway opening flows were measured via face mask-pneumotachograph (P-tach), whereas chest wall flows were derived from respiratory inductance plethysmography (RIP) excursions. Next, for each, we computed two spectral shape indexes: 1) harmonic distortion ( k d; k d,P-tachand k d,RIP, respectively) defines the extent to which flows deviated from a single sine wave, and 2) the exponent of the power law ( s; s P-tachand s RIP, respectively), describing the spectral energy vs. frequency. P-tach and RIP flow spectra exhibited similar power law functional forms consistently in all infants. Also, mouth [ s P-tach = 3.73 ± 0.23% (95% confidence interval), k d,P-tach = 38.8 ± 4.6%] and chest wall ( s RIP = 3.51 ± 0.30%, k d,RIP = 42.8 ± 4.8%) indexes were similar and highly correlated ( s RIP = 1.17 × s P-tach + 0.85; r 2 = 0.81; k d,RIP = 0.90 × k d,P-tach + 8.0; r 2 = 0.76). The corresponding time to peak tidal expiratory flow-to-expiratory time ratio (0.62 ± 0.08) was higher than reported in older infants. The obtained s and k d values are similar to those reported in older and/or larger chronic lung disease infants, yet appreciably lower than for 1-mo-old healthy infants of closer age and/or size; this indicated increased complexity of tidal flows in very low birth weight babies. Importantly, we found equivalent flow spectral data from mouth and chest wall tidal flows. The latter are desirable because they avoid face mask artificial effects, including leaks around it, they do not interfere with ventilatory support delivery, and they may facilitate longer measurements that are useful in control of breathing assessment.

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Brighton, B., S. Sherker, R. Brander, M. Thompson, and A. Bradstreet. "Rip current related drowning deaths and rescues in Australia 2004–2011." Natural Hazards and Earth System Sciences 13, no. 4 (April 22, 2013): 1069–75. http://dx.doi.org/10.5194/nhess-13-1069-2013.

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Abstract. Rip currents are a common hazard to beachgoers found on many beaches around the world, but it has proven difficult to accurately quantify the actual number of rip current related drowning deaths in many regions and countries. Consequently, reported estimates of rip current drowning can fluctuate considerably and are often based on anecdotal evidence. This study aims to quantify the incidence of rip current related drowning deaths and rescues in Australia from 2004 to 2011. A retrospective search was undertaken for fatal and non-fatal rip-related drowning incidents from Australia's National Coronial Information System (NCIS), Surf Life Saving Australia's (SLSA, 2005–2011) SurfGuard Incident Report Database (IRD), and Media Monitors for the period 1 July 2004 to 30 June 2011. In this time, rip currents were recorded as a factor in 142 fatalities of a total of 613 coastal drowning deaths (23.2%), an average of 21 per year. Rip currents were related to 44% of all beach-related drowning deaths and were involved in 57.4% of reported major rescues in Australian locations where rips occur. A comparison with international operational statistics over the same time period describes rip-related rescues as 53.7% of the total rescues in the US, 57.9% in the UK and 49.4% in New Zealand. The range 49–58% is much lower than 80–89% traditionally cited. The results reported are likely to underestimate the size of the rip current hazard, because we are limited by the completeness of data on rip-related events; however this is the most comprehensive estimate to date. Beach safety practitioners need improved data collection and standardized definitions across organisations. The collection of drowning data using consistent categories and the routine collection of rip current information will allow for more accurate global comparisons.

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Xiao, Yechen, Hongling Li, Jun Zhang, Andrew Volk, Shubin Zhang, Wei Wei, Shanshan Zhang, Peter Breslin, and Jiwang Zhang. "TNF-α/Fas-RIP-1–induced cell death signaling separates murine hematopoietic stem cells/progenitors into 2 distinct populations." Blood 118, no. 23 (December 1, 2011): 6057–67. http://dx.doi.org/10.1182/blood-2011-06-359448.

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AbstractWe studied the effects of TNF-α and Fas-induced death signaling in hematopoietic stem and progenitor cells (HSPCs) by examining their contributions to the development of bone marrow failure syndromes in Tak1-knockout mice (Tak1−/−). We found that complete inactivation of TNF-α signaling by deleting both of its receptors, 1 and 2 (Tnfr1−/−r2−/−), can prevent the death of 30% to 40% of Tak1−/− HSPCs and partially repress the bone marrow failure phenotype of Tak1−/− mice. Fas deletion can prevent the death of 5% to 10% of Tak1−/− HSPCs but fails to further improve the survival of Tak1−/−Tnfr1−/−r2−/− HSPCs, suggesting that Fas might induce death within a subset of TNF-α-sensitive HSPCs. This TNF-α/Fas-induced cell death is a type of receptor-interacting protein-1 (RIP-1)–dependent programmed necrosis called necroptosis, which can be prevented by necrostatin-1, a specific RIP-1 inhibitor. In addition, we found that the remaining Tak1−/− HSPCs died of apoptosis mediated by the caspase-8–dependent extrinsic apoptotic pathway. This apoptosis can be converted into necroptosis by the inhibition of caspase-8 and prevented by inhibiting both caspase-8 and RIP-1 activities. We concluded that HSPCs are heterogeneous populations in response to death signaling stimulation. Tak1 mediates a critical survival signal, which protects against both TNF-α/Fas-RIP-1–dependent necroptosis and TNF-α/Fas-independent apoptosis in HSPCs.

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Shen, Han-Ming, Yong Lin, Swati Choksi, Jamie Tran, Tian Jin, Lufen Chang, Michael Karin, Jianke Zhang, and Zheng-gang Liu. "Essential Roles of Receptor-Interacting Protein and TRAF2 in Oxidative Stress-Induced Cell Death." Molecular and Cellular Biology 24, no. 13 (July 1, 2004): 5914–22. http://dx.doi.org/10.1128/mcb.24.13.5914-5922.2004.

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ABSTRACT Oxidative stress and reactive oxygen species (ROS) can elicit and modulate various physiological and pathological processes, including cell death. However, the mechanisms controlling ROS-induced cell death are largely unknown. Data from this study suggest that receptor-interacting protein (RIP) and tumor necrosis factor receptor (TNFR)-associated factor 2 (TRAF2), two key effector molecules of TNF signaling, are essential for ROS-induced cell death. We found that RIP−/− or TRAF2−/− mouse embryonic fibroblasts (MEF) are resistant to ROS-induced cell death when compared to wild-type cells, and reconstitution of RIP and TRAF2 gene expression in their respective deficient MEF cells restored their sensitivity to H2O2-induced cell death. We also found that RIP and TRAF2 form a complex upon H2O2 exposure, but without the participation of TNFR1. The colocalization of RIP with a membrane lipid raft marker revealed a possible role of lipid rafts in the transduction of cell death signal initiated by H2O2. Finally, our results demonstrate that activation of c-Jun NH2-terminal kinase 1 is a critical event downstream of RIP and TRAF2 in mediating ROS-induced cell death. Therefore, our study uncovers a novel signaling pathway regulating oxidative stress-induced cell death.

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Thome, Margot, Kay Hofmann, Kim Burns, Fabio Martinon, Jean-Luc Bodmer, Chantal Mattmann, and Jürg Tschopp. "Identification of CARDIAK, a RIP-like kinase that associates with caspase-1." Current Biology 8, no. 15 (July 1998): 885–89. http://dx.doi.org/10.1016/s0960-9822(07)00352-1.

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Guay-Woodford, Lisa M. "RIP-ed and ready to dance: new mechanisms for polycystin-1 signaling." Journal of Clinical Investigation 114, no. 10 (November 15, 2004): 1404–6. http://dx.doi.org/10.1172/jci23544.

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Moulin, Maryline, Holly Anderton, Anne K. Voss, Tim Thomas, Wendy Wei-Lynn Wong, Aleksandra Bankovacki, Rebecca Feltham, et al. "IAPs limit activation of RIP kinases by TNF receptor 1 during development." EMBO Journal 31, no. 7 (February 10, 2012): 1679–91. http://dx.doi.org/10.1038/emboj.2012.18.

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Bersani, Cinzia, Mikael Huss, Stefania Giacomello, Li-Di Xu, Julie Bianchi, Sofi Eriksson, Fredrik Jerhammar, et al. "Genome-wide identification of Wig-1 mRNA targets by RIP-Seq analysis." Oncotarget 7, no. 2 (December 11, 2015): 1895–911. http://dx.doi.org/10.18632/oncotarget.6557.

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32

Rech, Cassiano Ricardo, Edio Luiz Petroski, Rosane Carla Rosendo da Silva, and João Carlos Nunes da Silva. "Indicadores antropométricos de excesso de gordura corporal em mulheres." Revista Brasileira de Medicina do Esporte 12, no. 3 (June 2006): 119–24. http://dx.doi.org/10.1590/s1517-86922006000300002.

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O objetivo deste estudo foi determinar a sensibilidade, a especificidade e a concordância entre dois indicadores de excesso de gordura em mulheres. Foram avaliadas 65 mulheres (50-77 anos de idade), com massa corporal média de 70,3 ± 11kg, estatura de 158,0 ± 5,5cm, permitindo o cálculo do índice de massa corporal (IMC) e do recíproco do índice ponderal (RIP). O percentual de gordura, mensurado através da absortometria radiológica de dupla energia (%G DEXA), foi utilizado como o método de referência. A estatística descritiva, a correlação de linear de Pearson (r) e o índice de Kappa (k) foram utilizados para análise dos dados. O IMC, o RIP e o %G DEXA apresentaram escores médios de 28 ± 4,2kg.m-2; 38 ± 1,9cm.kg-1/3; e 38,1 ± 6,0%, respectivamente. A prevalência de excesso de gordura foi de 89,2% para o %G DEXA. O RIP e o IMC apresentaram prevalências de excesso de gordura de 83,1% e 73,8%, respectivamente. Os coeficientes de correlação linear de Pearson entre %G DEXA e o RIP (r = -0,76) e entre %G DEXA e o IMC (r = 0,72) foram significativos (p < 0,01). O índice de Kappa identificou associação de k = 0,31 entre as medidas de %G DEXA e IMC, e de k = 0,48 entre %G DEXA e RIP. Os indicadores antropométricos apresentaram índices de sensibilidade e especificidade altos (IMC = 79,3% e 71,4%; RIP = 90% e 71,4% respectivamente). A análise através da curva ROC (receiver operator characteristic curve) apresentou áreas sobre a curva de 0,80 para o IMC e de 0,83 para o RIP que não diferiram significativamente (p < 0,05). Os pontos de corte de 26,2kg.m-2 para o IMC e 39,3cm.kg-1/3 para o RIP demonstraram a melhor relação entre sensibilidade e especificidade na identificação de excesso de gordura. Assim, conclui-se que os indicadores antropométricos analisados não diferem em relação à identificação de excesso de gordura e que ambos apresentam valores de sensibilidade e especificidade altos na avaliação do excesso de gordura em mulheres acima de 50 anos de idade.

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Mori, Hiroyuki, Ken Inoki, Darren Opland, Heike Münzberg, Eneida C. Villanueva, Miro Faouzi, Tsuneo Ikenoue, et al. "Critical roles for the TSC-mTOR pathway in β-cell function." American Journal of Physiology-Endocrinology and Metabolism 297, no. 5 (November 2009): E1013—E1022. http://dx.doi.org/10.1152/ajpendo.00262.2009.

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TSC1 is a tumor suppressor that associates with TSC2 to inactivate Rheb, thereby inhibiting signaling by the mammalian target of rapamycin (mTOR) complex 1 (mTORC1). mTORC1 stimulates cell growth by promoting anabolic cellular processes, such as translation, in response to growth factors and nutrient signals. To test roles for TSC1 and mTORC1 in β-cell function, we utilized Rip2/ Cre to generate mice lacking Tsc1 in pancreatic β-cells ( Rip-Tsc1cKO mice). Although obesity developed due to hypothalamic Tsc1 excision in older Rip-Tsc1cKO animals, young animals displayed a prominent gain-of-function β-cell phenotype prior to the onset of obesity. The young Rip-Tsc1cKO animals displayed improved glycemic control due to mTOR-mediated enhancement of β-cell size, mass, and insulin production but not determinants of β-cell number (proliferation and apoptosis), consistent with an important anabolic role for mTOR in β-cell function. Furthermore, mTOR mediated these effects in the face of impaired Akt signaling in β-cells. Thus, mTOR promulgates a dominant signal to promote β-cell/islet size and insulin production, and this pathway is crucial for β-cell function and glycemic control.

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Sala-Valdes, M., M. Gordon-Alonso, E. Tejera, A. Ibanez, J. R. Cabrero, A. Ursa, M. Mittelbrunn, F. Lozano, F. Sanchez-Madrid, and M. Yanez-Mo. "Association of syntenin-1 with M-RIP polarizes Rac-1 activation during chemotaxis and immune interactions." Journal of Cell Science 125, no. 5 (February 20, 2012): 1235–46. http://dx.doi.org/10.1242/jcs.094912.

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35

Driezen, Pete, Nigar Nargis, Mary E. Thompson, K. Michael Cummings, Geoffrey T. Fong, Frank J. Chaloupka, Ce Shang, and Kai-Wen Cheng. "State-Level Affordability of Factory-Made Cigarettes among Current US Smokers: Findings from the ITC US Survey, 2003–2015." International Journal of Environmental Research and Public Health 16, no. 13 (July 9, 2019): 2439. http://dx.doi.org/10.3390/ijerph16132439.

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Cigarette affordability measures the price smokers pay for cigarettes in relation to their incomes. Affordability can be measured using the relative income price of cigarettes (RIP), or the price smokers pay to purchase 100 packs of 20 cigarettes divided by their per capita household income. Using longitudinal data from 7046 smokers participating in the International Tobacco Control (ITC) US Survey, the purpose of this study was to test whether affordability significantly changed following the US federal tax increase implemented on 1 April 2009. This study also estimated temporal trends in affordability from 2003–2015 at state and national levels using small area estimation methods and segmented linear mixed effects regression models. RIP increased slightly during 2003–2008. This was followed by a 30% increase during 2008–2010, indicating cigarettes were less affordable after the federal tax increase. RIP continued to increase during 2010–2013 but decreased during 2013–2015, suggesting cigarettes have recently become more affordable for US smokers. State-level trends in RIP were consistent with overall national trends. Controlling for other factors, a $1 increase in the state excise tax was significantly associated with a 9% increase in RIP, indicating state taxes reduced affordability. Tax-induced price increases must keep pace with underlying economic conditions to ensure cigarettes do not become more affordable over time.

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Izumi, Kenneth M., Ellen Cahir McFarland, Adrian T. Ting, Elisabeth A. Riley, Brian Seed, and Elliott D. Kieff. "The Epstein-Barr Virus Oncoprotein Latent Membrane Protein 1 Engages the Tumor Necrosis Factor Receptor-Associated Proteins TRADD and Receptor-Interacting Protein (RIP) but Does Not Induce Apoptosis or Require RIP for NF-κB Activation." Molecular and Cellular Biology 19, no. 8 (August 1, 1999): 5759–67. http://dx.doi.org/10.1128/mcb.19.8.5759.

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ABSTRACT A site in the Epstein-Barr virus (EBV) transforming protein LMP1 that constitutively associates with the tumor necrosis factor receptor 1 (TNFR1)-associated death domain protein TRADD to mediate NF-κB and c-Jun N-terminal kinase activation is critical for long-term lymphoblastoid cell proliferation. We now find that LMP1 signaling through TRADD differs from TNFR1 signaling through TRADD. LMP1 needs only 11 amino acids to activate NF-κB or synergize with TRADD in NF-κB activation, while TNFR1 requires ∼70 residues. Further, LMP1 does not require TRADD residues 294 to 312 for NF-κB activation, while TNFR1 requires TRADD residues 296 to 302. LMP1 is partially blocked for NF-κB activation by a TRADD mutant consisting of residues 122 to 293. Unlike TNFR1, LMP1 can interact directly with receptor-interacting protein (RIP) and stably associates with RIP in EBV-transformed lymphoblastoid cell lines. Surprisingly, LMP1 does not require RIP for NF-κB activation. Despite constitutive association with TRADD or RIP, LMP1 does not induce apoptosis in EBV-negative Burkitt lymphoma or human embryonic kidney 293 cells. These results add a different perspective to the molecular interactions through which LMP1, TRADD, and RIP participate in B-lymphocyte activation and growth.

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Kilpatrick, Laurie E., Shuang Sun, and Helen M. Korchak. "Selective regulation by δ-PKC and PI 3-kinase in the assembly of the antiapoptotic TNFR-1 signaling complex in neutrophils." American Journal of Physiology-Cell Physiology 287, no. 3 (September 2004): C633—C642. http://dx.doi.org/10.1152/ajpcell.00486.2003.

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TNF is implicated in the attenuation of neutrophil constitutive apoptosis during sepsis. Antiapoptotic signaling is mediated principally through the TNF receptor-1 (TNFR-1). In adherent neutrophils, when β-integrin signaling is activated, TNF phosphorylates TNFR-1 and activates prosurvival and antiapoptotic signaling. Previously, we identified the δ-PKC isotype and phosphatidylinositol (PI) 3-kinase as critical regulators of TNF signaling in adherent neutrophils. Both kinases associate with TNFR-1 in response to TNF and are required for TNFR-1 serine phosphorylation, NF-κB activation, and inhibition of apoptosis. The purpose of this study was to examine the role of δ-PKC and PI 3-kinase in the assembly of TNFR-1 signaling complex that regulates NF-κB activation and antiapoptotic signaling. Coimmunoprecipitation studies established that PI 3-kinase, δ-PKC, and TNFR-1 formed a signal complex in response to TNF. δ-PKC recruitment required both δ-PKC and PI 3-kinase activity, whereas PI 3-kinase recruitment was δ-PKC independent, suggesting that PI 3-kinase acts upstream of δ-PKC. An important regulatory step in control of antiapoptotic signaling is the assembly of the TNFR-1-TNFR-1-associated death domain protein (TRADD)-TNFR-associated factor 2 (TRAF2)-receptor interacting protein (RIP) complex that controls NF-κB activation. Inhibition of either δ-PKC or PI 3-kinase decreased TNF-mediated recruitment of RIP and TRAF2 to TNFR-1. In contrast, TRADD recruitment was enhanced. Thus δ-PKC and PI 3-kinase are positive regulators of TNF-mediated association of TRAF2 and RIP with TNFR-1. Conversely, these kinases are negative regulators of TRADD association. These results suggest that δ-PKC and PI 3-kinase regulate TNF antiapoptotic signaling at the level of the TNFR-1 through control of assembly of a TNFR-1-TRADD-RIP-TRAF2 complex.

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Ida, Yosuke, Megumi Watanabe, Hiroshi Ohguro, and Fumihito Hikage. "Simultaneous Use of ROCK Inhibitors and EP2 Agonists Induces Unexpected Effects on Adipogenesis and the Physical Properties of 3T3-L1 Preadipocytes." International Journal of Molecular Sciences 22, no. 9 (April 28, 2021): 4648. http://dx.doi.org/10.3390/ijms22094648.

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To elucidate the additive effects of an EP2 agonist, omidenepag (OMD) or butaprost (Buta) on the Rho-associated coiled-coil-containing protein kinase (ROCK) inhibitor, ripasudil (Rip) on adipose tissue, two- or three-dimension (2D or 3D) cultures of 3T3-L1 cells were analyzed by lipid staining, the mRNA expression of adipogenesis-related genes, extracellular matrix (ECM) molecules including collagen (Col) -1, -4 and -6, and fibronectin (Fn), and the sizes and physical properties of 3D organoids, as measured by a micro-squeezer. The results indicate that adipogenesis induced (1) an enlargement of the 3D organoids; (2) a substantial enhancement in lipid staining as well as the expression of the Pparγ, Ap2 and Leptin genes; (3) a significant softening of the 3D organoids, the effects of which were all enhanced by Rip except for Pparγ expression; and (4) a significant downregulation in Col1 and Fn, and a significant upregulation in Col4, Col6, the effects of which were unchanged by Rip. When adding the EP2 agonist to Rip, (1) the sizes of the 3D organoids were reduced substantially; (2) lipid staining was increased (OMD), or decreased (Buta); (3) the stiffness of the 3D organoids was substantially increased in Buta; (4-1) the expression of Pparγ was suppressed (2D, OMD) or increased (2D, Buta), and the expressions of Ap2 were downregulated (2D, 3D) and Leptin was increased (2D) or decreased (3D), (4-2) all the expressions of four ECM molecules were upregulated in 2D (2D), and in 3D, the expression of Col1, Col4 was upregulated. The collective findings reported herein indicate that the addition of an EP2 agonist, OMD or Buta significantly but differently modulate the Rip-induced effects on adipogenesis and the physical properties of 2D and 3D cultured 3T3-L1 cells.

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Fiksen-Olsen, M. J., and J. C. Romero. "Renal effects of prostaglandin inhibition during increases in renal venous pressure." American Journal of Physiology-Renal Physiology 260, no. 4 (April 1, 1991): F525—F529. http://dx.doi.org/10.1152/ajprenal.1991.260.4.f525.

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The role of prostaglandins (PGs) in mediating the hemodynamic and natriuretic responses to increases in renal interstitial pressure (RIP) induced by altering renal venous pressure (RVP) from control (3.6 +/- 0.6) to 15 and 30 mmHg was examined before and after PG inhibition in pentobarbital sodium-anesthetized dogs. These elevations of RVP resulted in RIP increasing from control (6 +/- 1) to 11 +/- 1 and 23 +/- 2 mmHg, respectively, without altering mean arterial pressure (MAP), renal blood flow (RBF), and glomerular filtration rate (GFR). Sodium excretion increased only when RVP reached 30 mmHg. During the inhibition of PG synthesis, 15 mmHg RVP induced a 10% decrease in RBF, and 30 mmHg RVP induced a further 20% decrease in RBF and a 50% decrease in GFR. PG synthesis inhibition did not alter either the RIP or the sodium excretory response. In conclusion, the natriuresis associated with the RIP increases induced by increasing RVP appears to be independent of PG synthesis. PGs, however, appear to be important for the maintenance of RBF and GFR during increased RVP. These findings suggest that different mechanisms are involved in the hemodynamic and natriuretic responses to arterial vs. venous pressure changes.

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Tsibulnikov, Sergey Y., Leonid N. Maslov, Alexander S. Gorbunov, Nikita S. Voronkov, Alla A. Boshchenko, Sergey V. Popov, Ekaterina S. Prokudina, Nirmal Singh, and James M. Downey. "A Review of Humoral Factors in Remote Preconditioning of the Heart." Journal of Cardiovascular Pharmacology and Therapeutics 24, no. 5 (April 29, 2019): 403–21. http://dx.doi.org/10.1177/1074248419841632.

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A humoral mechanism of cardioprotection by remote ischemic preconditioning (RIP) has been clearly demonstrated in various models of ischemia–reperfusion including upper and lower extremities, liver, and the mesenteric and renal arteries. A wide range of humoral factors for RIP have been proposed including hydrophobic peptides, opioid peptides, adenosine, prostanoids, endovanilloids, endocannabinoids, calcitonin gene-related peptide, leukotrienes, noradrenaline, adrenomedullin, erythropoietin, apolipoprotein, A-I glucagon-like peptide-1, interleukin 10, stromal cell-derived factor 1, and microRNAs. Virtually, all of the components of ischemic preconditioning’s signaling pathway such as nitric oxide synthase, protein kinase C, redox signaling, PI3-kinase/Akt, glycogen synthase kinase β, ERK1/2, mitoKATPchannels, Connexin 43, and STAT were all found to play a role. The signaling pattern also depends on which remote vascular bed was subjected to ischemia and on the time between applying the rip and myocardial ischemia occurs. Because there is convincing evidence for many seemingly diverse humoral components in RIP, the most likely explanation is that the overall mechanism is complex like that seen in ischemic preconditioning where multiple components are both in series and in parallel and interact with each other. Inhibition of any single component in the right circumstance may block the resulting protective effect, and selectively activating that component may trigger the protection. Identifying the humoral factors responsible for RIP might be useful in developing drugs that confer RIP’s protection in a more comfortable and reliable manner.

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Watson, H. L., D. A. Poole, and M. A. Sackner. "Accuracy of respiratory inductive plethysmographic cross-sectional areas." Journal of Applied Physiology 65, no. 1 (July 1, 1988): 306–8. http://dx.doi.org/10.1152/jappl.1988.65.1.306.

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The present study was undertaken to evaluate whether the respiratory inductive plethysmograph (RIP) 1) reflects changes of cross-sectional area enclosed by its transducer band in the presence of deformations of shape or whether it 2) has a stable base line. Testing of RIP was carried out with a device incorporating a thermally compensated oscillator and digital demodulatory circuitry. This system, introduced to commerce in 1983, superceded the nonthermal compensated oscillatory and analog demodulator circuitry first used in 1977. Testing the effects of changing cross-sectional area was accomplished by stretching a standard RIP transducer band around wooden dowels placed in holes on a peg board grid to form 23 curved and 5 rectangular shapes. The output voltage from RIP was linear for both the curved and rectangular shapes for changes of cross-sectional area within a physiological range. However, the regression line of voltage vs. cross-sectional area for the rectangular shapes was parallel and slightly displaced from the regression line for the curved shapes due to mutual coupling of inductance in the corners. Base-line drift from a RIP transducer band stretched to enclose an elliptical shape was less than 2.5 mV over a 12-h observation period. Current RIP technology accurately reflects changes of cross-sectional area of physiological shapes and has a stable base line.

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Geng, Pengbo, Wengu Chen, and Huanmin Ge. "Perturbation Analysis of Orthogonal Least Squares." Canadian Mathematical Bulletin 62, no. 4 (March 22, 2019): 780–97. http://dx.doi.org/10.4153/s0008439519000134.

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AbstractThe Orthogonal Least Squares (OLS) algorithm is an efficient sparse recovery algorithm that has received much attention in recent years. On one hand, this paper considers that the OLS algorithm recovers the supports of sparse signals in the noisy case. We show that the OLS algorithm exactly recovers the support of $K$-sparse signal $\boldsymbol{x}$ from $\boldsymbol{y}=\boldsymbol{\unicode[STIX]{x1D6F7}}\boldsymbol{x}+\boldsymbol{e}$ in $K$ iterations, provided that the sensing matrix $\boldsymbol{\unicode[STIX]{x1D6F7}}$ satisfies the restricted isometry property (RIP) with restricted isometry constant (RIC) $\unicode[STIX]{x1D6FF}_{K+1}<1/\sqrt{K+1}$, and the minimum magnitude of the nonzero elements of $\boldsymbol{x}$ satisfies some constraint. On the other hand, this paper demonstrates that the OLS algorithm exactly recovers the support of the best $K$-term approximation of an almost sparse signal $\boldsymbol{x}$ in the general perturbations case, which means both $\boldsymbol{y}$ and $\boldsymbol{\unicode[STIX]{x1D6F7}}$ are perturbed. We show that the support of the best $K$-term approximation of $\boldsymbol{x}$ can be recovered under reasonable conditions based on the restricted isometry property (RIP).

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Northington, Frances J., Raul Chavez-Valdez, Ernest M. Graham, Sheila Razdan, Estelle B. Gauda, and Lee J. Martin. "Necrostatin Decreases Oxidative Damage, Inflammation, and Injury after Neonatal HI." Journal of Cerebral Blood Flow & Metabolism 31, no. 1 (June 23, 2010): 178–89. http://dx.doi.org/10.1038/jcbfm.2010.72.

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Necrostatin-1 inhibits receptor-interacting protein (RIP)-1 kinase and programmed necrosis and is neuroprotective in adult rodent models. Owing to the prominence of necrosis and continuum cell death in neonatal hypoxia–ischemia (HI), we tested whether necrostatin was neuroprotective in the developing brain. Postnatal day (P)7 mice were exposed to HI and injected intracerebroventricularly with 0.1 μL of 80 μmol necrostatin, Nec-1, 5-(1H-Indol-3-ylmethyl)-(2-thio-3-methyl) hydantoin, or vehicle. Necrostatin significantly decreased injury in the forebrain and thalamus at P11 and P28. There was specific neuroprotection in necrostatin-treated males. Necrostatin treatment decreased necrotic cell death and increased apoptotic cell death. Hypoxia–ischemia enforced RIP1–RIP3 complex formation and inhibited RIP3–FADD (Fas-associated protein with death domain) interaction, and these effects were blocked by necrostatin. Necrostatin also decreased HI-induced oxidative damage to proteins and attenuated markers of inflammation coincidental with decreased nuclear factor-κB and caspase 1 activation, and FLIP ((Fas-associated death-domain-like IL-1β-converting enzyme)-inhibitory protein) gene and protein expression. In this model of severe neonatal brain injury, we find that cellular necrosis can be managed therapeutically by a single dose of necrostatin, administered after HI, possibly by interrupting RIP1–RIP3-driven oxidative injury and inflammation. The effects of necrostatin treatment after HI reflect the importance of necrosis in the delayed phases of neonatal brain injury and represent a new direction for therapy of neonatal HI.

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Han, Weidong, Jiansheng Xie, Yong Fang, Zhanggui Wang, and Hongming Pan. "Nec-1 Enhances Shikonin-Induced Apoptosis in Leukemia Cells by Inhibition of RIP-1 and ERK1/2." International Journal of Molecular Sciences 13, no. 6 (June 12, 2012): 7212–25. http://dx.doi.org/10.3390/ijms13067212.

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Geng, Lele, Gai Zhang, Min Yao, and Yong Fang. "Rip 1-dependent endothelial necroptosis participates in ischemia-reperfusion injury of mouse flap." Journal of Dermatological Science 97, no. 1 (January 2020): 30–40. http://dx.doi.org/10.1016/j.jdermsci.2019.11.009.

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46

Wang, Yao, and Jianjun Wang. "Improved RIP Conditions for Compressed Sensing with Coherent Tight Frames." Discrete Dynamics in Nature and Society 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/4372080.

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This paper establishes new sufficient conditions on the restricted isometry property (RIP) for compressed sensing with coherent tight frames. One of our main results shows that the RIP (adapted to D) condition δk+θk,k<1 guarantees the stable recovery of all signals that are nearly k-sparse in terms of a coherent tight frame D via the l1-analysis method, which improves the existing ones in the literature.

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47

Susan Wong, F., Irene Visintin, Li Wen, Jennifer Granata, Richard Flavell, and Charles A. Janeway. "The Role of Lymphocyte Subsets in Accelerated Diabetes in Nonobese Diabetic–Rat Insulin Promoter–B7-1 (NOD-RIP-B7-1) Mice." Journal of Experimental Medicine 187, no. 12 (June 15, 1998): 1985–93. http://dx.doi.org/10.1084/jem.187.12.1985.

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B7-1 transgene expression on the pancreatic islets in nonobese diabetic (NOD) mice leads to accelerated diabetes, with >50% of animals developing diabetes before 12 wk of age. The expression of B7-1 directly on the pancreatic β cells, which do not normally express costimulator molecules, converts the cells into effective antigen-presenting cells leading to an intensified autoimmune attack. The pancreatic islet infiltrate in diabetic mice consists of CD8 T cells, CD4 T cells, and B cells, similar to diabetic nontransgenic NOD mice. To elucidate the relative importance of each of the subsets of cells, the NOD–rat insulin promoter (RIP)-B7-1 animals were crossed with NOD.β2microglobulin −/− mice which lack major histocompatibility complex class I molecules and are deficient in peripheral CD8 T cells, NOD.CD4 −/− mice which lack T cells expressing CD4, and NOD.μMT −/− mice which lack B220-positive B cells. These experiments showed that both CD4 and CD8 T cells were necessary for the accelerated onset of diabetes, but that B cells, which are needed for diabetes to occur in normal NOD mice, are not required. It is possible that B lymphocytes play an important role in the provision of costimulation in NOD mice which is unnecessary in the NOD-RIP-B7-1 transgenic mice.

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Vijayaraghavan, Y., and M. Kapoor. "Disruption of the NAD+-specific glutamate dehydrogenase gene of Neurospora crassa by means of the RIP (repeat-induced point mutations) process." Biochemistry and Cell Biology 74, no. 1 (January 1, 1996): 29–40. http://dx.doi.org/10.1139/o96-004.

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The structural gene for the catabolite-repressed, substrate-induced NAD+-specifïc glutamate dehydrogenase (gdh-1) of Neurospora crassa was disrupted using the process of repeat-induced point mutation (RIP). Plasmids containing incomplete copies of the gene, along with selectable markers, were introduced into germinated conidia by electroporation. The sexual progeny of a transformant containing an ectopically integrated copy of a plasmid, harbouring the 5′ flanking region and a part of the coding sequence of gdh-1 DNA, was examined for the occurrence of RIP by (i) Southern blot analysis of the genomic DNA digested with the isoschizomers MboI and Sau3A, (ii) Northern blot analysis of total RNA in cultures subjected to repression and induction conditions for NAD–GDH, (iii) direct assessment of enzymatic activity, and (iv) evaluation of protein levels by Western blot analysis using a polyclonal anti-GDH IgG preparation. Attempts were made at delineating different regions of the gene exhibiting RIP by using 32P-labelled DNA probes, corresponding to (i) the complete gene, (ii) a fragment containing the 5′ flanking region plus two-thirds of the coding sequence, and (iii) the 5′ flanking segment alone. The extent and relative location of RIP, as revealed by these hybridization probes, appeared to correlate with changes in specific activity under repression and derepression conditions. Mutant progeny, thus recovered, included isolates with altered regulatory features, such as constitutive expression, inability to elicit derepression, higher-than-wildtype GDH levels under derepression and inefficient repression.Key words: glutamate dehydrogenase, Neurospora, repeat-induced point mutations, RIP, regulatory mutants.

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Linser, Rasmus, Nicola Salvi, Rodolfo Briones, Petra Rovó, Bert L. de Groot, and Gerhard Wagner. "The membrane anchor of the transcriptional activator SREBP is characterized by intrinsic conformational flexibility." Proceedings of the National Academy of Sciences 112, no. 40 (September 21, 2015): 12390–95. http://dx.doi.org/10.1073/pnas.1513782112.

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Regulated intramembrane proteolysis (RIP) is a conserved mechanism crucial for numerous cellular processes, including signaling, transcriptional regulation, axon guidance, cell adhesion, cellular stress responses, and transmembrane protein fragment degradation. Importantly, it is relevant in various diseases including Alzheimer’s disease, cardiovascular diseases, and cancers. Even though a number of structures of different intramembrane proteases have been solved recently, fundamental questions concerning mechanistic underpinnings of RIP and therapeutic interventions remain. In particular, this includes substrate recognition, what properties render a given substrate amenable for RIP, and how the lipid environment affects the substrate cleavage. Members of the sterol regulatory element-binding protein (SREBP) family of transcription factors are critical regulators of genes involved in cholesterol/lipid homeostasis. After site-1 protease cleavage of the inactive SREBP transmembrane precursor protein, RIP of the anchor intermediate by site-2 protease generates the mature transcription factor. In this work, we have investigated the labile anchor intermediate of SREBP-1 using NMR spectroscopy. Surprisingly, NMR chemical shifts, site-resolved solvent exposure, and relaxation studies show that the cleavage site of the lipid-signaling protein intermediate bears rigid α-helical topology. An evolutionary conserved motif, by contrast, interrupts the secondary structure ∼9–10 residues C-terminal of the scissile bond and acts as an inducer of conformational flexibility within the carboxyl-terminal transmembrane region. These results are consistent with molecular dynamics simulations. Topology, stability, and site-resolved dynamics data suggest that the cleavage of the α-helical substrate in the case of RIP may be associated with a hinge motion triggered by the molecular environment.

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Bao, Shunzhong, David A. Jacobson, Mary Wohltmann, Alan Bohrer, Wu Jin, Louis H. Philipson, and John Turk. "Glucose homeostasis, insulin secretion, and islet phospholipids in mice that overexpress iPLA2β in pancreatic β-cells and in iPLA2β-null mice." American Journal of Physiology-Endocrinology and Metabolism 294, no. 2 (February 2008): E217—E229. http://dx.doi.org/10.1152/ajpendo.00474.2007.

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Studies with genetically modified insulinoma cells suggest that group VIA phospholipase A2 (iPLA2β) participates in amplifying glucose-induced insulin secretion. INS-1 insulinoma cells that overexpress iPLA2β, for example, exhibit amplified insulin-secretory responses to glucose and cAMP-elevating agents. To determine whether similar effects occur in whole animals, we prepared transgenic (TG) mice in which the rat insulin 1 promoter (RIP) drives iPLA2β overexpression, and two characterized TG mouse lines exhibit similar phenotypes. Their pancreatic islet iPLA2β expression is increased severalfold, as reflected by quantitative PCR of iPLA2β mRNA, immunoblotting of iPLA2β protein, and iPLA2β enzymatic activity. Immunofluorescence microscopic studies of pancreatic sections confirm iPLA2β overexpression in RIP-iPLA2β-TG islet β-cells without obviously perturbed islet morphology. Male RIP-iPLA2β-TG mice exhibit lower blood glucose and higher plasma insulin concentrations than wild-type (WT) mice when fasting and develop lower blood glucose levels in glucose tolerance tests, but WT and TG blood glucose levels do not differ in insulin tolerance tests. Islets from male RIP-iPLA2β-TG mice exhibit greater amplification of glucose-induced insulin secretion by a cAMP-elevating agent than WT islets. In contrast, islets from male iPLA2β-null mice exhibit blunted insulin secretion, and those mice have impaired glucose tolerance. Arachidonate incorporation into and the phospholipid composition of RIP-iPLA2β-TG islets are normal, but they exhibit reduced Kv2.1 delayed rectifier current and prolonged glucose-induced action potentials and elevations of cytosolic Ca2+ concentration that suggest a molecular mechanism for the physiological role of iPLA2β to amplify insulin secretion.

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Journal articles on the topic 'RIP-1'

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