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Journal articles on the topic 'Siah'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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1

Li, Qiang, Ping Wang, Keqiang Ye, and Hua Cai. "Central role of SIAH inhibition in DCC-dependent cardioprotection provoked by netrin-1/NO." Proceedings of the National Academy of Sciences 112, no. 3 (January 5, 2015): 899–904. http://dx.doi.org/10.1073/pnas.1420695112.

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Deleted in colorectal cancer (DCC), a large transmembrane receptor of netrin-1, is critical for mediating netrin-1’s cardioprotective function. In the present study we investigated novel mechanisms underlying netrin-1–induced, rapid, and feed-forward up-regulation of DCC, which is believed to sustain nitric oxide (NO) production to potentiate cardioprotection. Intriguingly, NO markedly reduced expression of the E3 ubiquitin ligase seven in absentia homolog (SIAH) that is specific for regulation of protesome-dependent DCC degradation, resulting in accumulation of DCC. The two SIAH isoforms compensate for each other when one is repressed; inhibition of both SIAH1 and SIAH2 using combined siRNAs significantly reduced infarct size while improving cardiac function after ischemia/reperfusion injury of the heart. This effect was absent in DCC-deficient mice. Moreover, in vivo RNAi inhibition of SIAH1/2 further augmented netrin-1’s cardioprotective function. In summary, these data identify a novel therapeutic target of SIAH in facilitating NO/netrin-1–dependent cardioprotection, using the DCC receptor. Combination of netrin-1 and SIAH RNAi may prove to be a substantially effective therapy for myocardial infarction.

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2

Frew, Ian J., Ross A. Dickins, Andrew R. Cuddihy, Merci Del Rosario, Christoph Reinhard, Matthew J. O'Connell, and David D. L. Bowtell. "Normal p53 Function in Primary Cells Deficient for Siah Genes." Molecular and Cellular Biology 22, no. 23 (December 1, 2002): 8155–64. http://dx.doi.org/10.1128/mcb.22.23.8155-8164.2002.

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ABSTRACT Overexpression studies have suggested that Siah1 proteins may act as effectors of p53-mediated cellular responses and as regulators of mitotic progression. We have tested these hypotheses using Siah gene knockout mice. Siah1a and Siah1b were not induced by activation of endogenous p53 in tissues, primary murine embryonic fibroblasts (MEFs) or thymocytes. Furthermore, primary MEFs lacking Siah1a, Siah1b, Siah2, or both Siah2 and Siah1a displayed normal cell cycle progression, proliferation, p53-mediated senescence, and G1 phase cell cycle arrest. Primary thymocytes deficient for Siah1a, Siah2, or both Siah2 and Siah1a, E1A-transformed MEFs lacking Siah1a, Siah1b, or Siah2, and Siah1b-null ES cells all underwent normal p53-mediated apoptosis. Finally, inhibition of Siah1b expression in Siah2 Siah1a double-mutant cells failed to inhibit cell division, p53-mediated induction of p21 expression, or cell cycle arrest. Our loss-of-function experiments do not support a general role for Siah genes in p53-mediated responses or mitosis.

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3

Hu, Gang, and Eric R. Fearon. "Siah-1 N-Terminal RING Domain Is Required for Proteolysis Function, and C-Terminal Sequences Regulate Oligomerization and Binding to Target Proteins." Molecular and Cellular Biology 19, no. 1 (January 1, 1999): 724–32. http://dx.doi.org/10.1128/mcb.19.1.724.

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ABSTRACT The Drosophila seven in absentia (sina) gene was initially discovered because its inactivation leads to R7 photoreceptor defects. Recent data indicate that Sina binds to the Sevenless pathway protein Phyllopod, and together they mediate degradation of Tramtrack, a transcriptional repressor of R7 cell fate. Independent studies have shown that Sina and its highly related mammalian homologues Siah-1 and Siah-2 bind to the DCC (deleted in colorectal cancer) protein and promote its proteolysis via the ubiquitin-proteasome pathway. To determine the roles of mammalian Siahs in proteolysis and their interactions with target proteins, we sought to define Siah-1 domains critical for regulation of DCC. Mutant Siah-1 proteins, harboring missense mutations in the carboxy (C)-terminal domain analogous to those present in Drosophila sinaloss-of-function alleles, failed to promote DCC degradation. Point mutations and deletion of the amino (N)-terminal RING finger domain of Siah-1 abrogated its ability to promote DCC proteolysis. In the course of defining Siah-1 sequences required for DCC degradation, we found that Siah-1 is itself rapidly degraded via the proteasome pathway, and RING domain mutations stabilized the Siah-1 protein. Siah-1 was found to oligomerize with itself and other Sina and Siah proteins via C-terminal sequences. Finally, evidence that endogenous Siah-1 regulates DCC proteolysis in cells was obtained through studies of an apparent dominant negative mutant of Siah-1, as well as via an antisense approach. The data indicate that the Siah-1 N-terminal RING domain is required for its proteolysis function, while the C-terminal sequences regulate oligomerization and binding to target proteins, such as DCC.

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4

Gupte, Girish R., and R. Prasad. "Geometries and Vibrational Spectra of Small Hydrogenated Silicon Clusters." International Journal of Modern Physics B 12, no. 16n17 (July 10, 1998): 1737–50. http://dx.doi.org/10.1142/s021797929800096x.

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We report a systematic study of ground state structures, vibrational spectra, cohesive energies and HOMO-LUMO gaps of small Si n H clusters (n=3, 10) based on the nonorthogonal tight-binding molecular dynamics scheme. The ground state structures have been obtained by using simulated annealing. In particular, we focus on how the addition of a hydrogen atom affects the ground state geometry and the stability of a Si n cluster. We find that hydrogen either enters into the surface of the cluster or occupies a position outside the cluster. In the first case, it drastically distorts the cluster, while in the latter, there is very little distortion. We find that in some cases Si n H cluster has some resemblance with Si n+1 cluster. We also find that hydrogen can form bonds with more than one silicon atom. Our calculation indicates that SiH, Si3H and Si5H will be more stable and Si4H , Si6H , Si7H , Si9H and Si10H will be less stable clusters.

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5

Frew, Ian J., Vicki E. Hammond, Ross A. Dickins, Julian M. W. Quinn, Carl R. Walkley, Natalie A. Sims, Ralf Schnall, et al. "Generation and Analysis of Siah2 Mutant Mice." Molecular and Cellular Biology 23, no. 24 (December 15, 2003): 9150–61. http://dx.doi.org/10.1128/mcb.23.24.9150-9161.2003.

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ABSTRACT Siah proteins function as E3 ubiquitin ligase enzymes to target the degradation of diverse protein substrates. To characterize the physiological roles of Siah2, we have generated and analyzed Siah2 mutant mice. In contrast to Siah1a knockout mice, which are growth retarded and exhibit defects in spermatogenesis, Siah2 mutant mice are fertile and largely phenotypically normal. While previous studies implicate Siah2 in the regulation of TRAF2, Vav1, OBF-1, and DCC, we find that a variety of responses mediated by these proteins are unaffected by loss of Siah2. However, we have identified an expansion of myeloid progenitor cells in the bone marrow of Siah2 mutant mice. Consistent with this, we show that Siah2 mutant bone marrow produces more osteoclasts in vitro than wild-type bone marrow. The observation that combined Siah2 and Siah1a mutation causes embryonic and neonatal lethality demonstrates that the highly homologous Siah proteins have partially overlapping functions in vivo.

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6

Della, N. G., P. V. Senior, and D. D. Bowtell. "Isolation and characterisation of murine homologues of the Drosophila seven in absentia gene (sina)." Development 117, no. 4 (April 1, 1993): 1333–43. http://dx.doi.org/10.1242/dev.117.4.1333.

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The seven in absentia gene (sina) is required for formation of the R7 photoreceptor cell in the developing eye of Drosophila melanogaster. The sina protein contains a putative zinc finger domain and localises to the cell nucleus in Drosophila. We report here the identification of a family of genes in the mouse (designated Siah) with extensive sequence homology to Drosophila sina. The Siah genes fall into two main groups: Siah-1, which consists of four closely related members, two of which appear to be functional, and Siah-2, which contains a single functional member. The predicted Siah proteins show an unusually high degree of conservation with sina over the majority of their lengths, diverging significantly only at their amino terminal ends. The Siah-1 and Siah-2 genes are widely expressed at a low level in the embryo and adult. Analysis of Siah-2 by hybridisation histochemistry shows that it is expressed at a higher level in a restricted number of sites during development, including the olfactory epithelium, retina, forebrain and proliferating cartilage of developing bone. The striking degree of sequence homology observed between the Drosophila and murine genes implies strong conservation pressure on the Siah genes and suggests that they play a significant role in vertebrate development.

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7

Briant, Douglas J., Derek F. Ceccarelli, and Frank Sicheri. "I Siah Substrate!" Structure 14, no. 4 (April 2006): 627–28. http://dx.doi.org/10.1016/j.str.2006.03.003.

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8

Moghayedi, Alireza, Bankole Awuzie, Temitope Omotayo, Karen Le Jeune, Mark Massyn, Christiana Okobi Ekpo, Manfred Braune, and Paimaan Byron. "A Critical Success Factor Framework for Implementing Sustainable Innovative and Affordable Housing: A Systematic Review and Bibliometric Analysis." Buildings 11, no. 8 (July 23, 2021): 317. http://dx.doi.org/10.3390/buildings11080317.

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The actualization of affordable housing remains a challenge. This challenge is exacerbated by the increasing societal demand for the incorporation of sustainability principles into such housing types to improve levels of occupant health and well-being whilst avouching the desired levels of affordability. Innovative technologies and practices have been described as beneficial to the effectuation of sustainable affordable housing. However, knowledge concerning the deployment of innovative technologies and practices in sustainable affordable housing (sustainable, innovative, affordable housing—SIAH) delivery remains nascent. Consequently, there is a lack of a common ontology among stakeholders concerning how to realize SIAH. This study aims to contribute toward the development of this body of knowledge through the establishment of the critical success factors (CSFs) for effective SIAH implementation. To achieve this objective, a systematic review and bibliometric analysis focusing on a juxtaposition of sustainable, innovative and affordable housing concepts was carried out based on the relevant literature. This led to the identification and clustering of CSFs for these housing concepts at individual levels and as a collective (SIAH). The findings of the study consisted of the establishment of four distinct yet interrelated facets through which SIAH can be achieved holistically, namely, housing design, house element, housing production method and housing technology. A total of 127 CSFs were found to be aligned to these facets, subsequently clustered, and conclusively used for the development of a SIAH CSF framework. The most frequently occurring CSFs with predominant interconnections were the utilization of energy-efficient systems/fittings, tenure security, a comfortable and healthy indoor environment, affordable housing price in relation to income and using water-efficient systems/fittings CSFs, and establishing the emergent SIAH CSF framework. The framework in this study is useful in the documentation of SIAH features for construction projects and further studies into SIAH CSFs.

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9

Samartsev, V. A., V. A. Gavrilov, and B. S. Pushkarev. "INTRAABDOMINAL HYPERTENSION SYNDROME: CURRENT STATE OF THE PROBLEM." Surgical practice, no. 2 (September 10, 2020): 35–42. http://dx.doi.org/10.38181/2223-2427-2020-2-35-42.

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Syndrome of intra-abdominal hypertension (SIAH) is a dangerous complication that can occur in patients with a surgical profile after surgery in the abdominal cavity. Only in the past 25 years has the SIAH been recognized. According to W. Ertel et al., In one third of patients with peritonitis, pancreatic necrosis, injuries of the abdominal cavity and after extensive surgery, there is an increase in intra-abdominal pressure (IAP), while SIAH develops in 5.5% of such patients. Mortality in SIAH is 42–68%. The reason for the development of so many deaths is the presence of diagnostic, preventive and therapeutic measures, as well as differences in the interpretation of terms. Today, much attention is paid to the study of SIAH, official attempts are being made to standardize and define terms and recommended methods of treatment, but this problem needs further study. The review presents data on the current state of the problem, current trends in the diagnosis, prevention and treatment of patients with IAP and SIAH, their use in practical research.

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10

Poh, Wee-Han, Jianqing Lin, Brendan Colley, Nicolai Müller, Boon Chong Goh, David Schleheck, Abbas El Sahili, et al. "The SiaABC threonine phosphorylation pathway controls biofilm formation in response to carbon availability in Pseudomonas aeruginosa." PLOS ONE 15, no. 11 (November 6, 2020): e0241019. http://dx.doi.org/10.1371/journal.pone.0241019.

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The critical role of bacterial biofilms in chronic human infections calls for novel anti-biofilm strategies targeting the regulation of biofilm development. However, the regulation of biofilm development is very complex and can include multiple, highly interconnected signal transduction/response pathways, which are incompletely understood. We demonstrated previously that in the opportunistic, human pathogen P. aeruginosa, the PP2C-like protein phosphatase SiaA and the di-guanylate cyclase SiaD control the formation of macroscopic cellular aggregates, a type of suspended biofilms, in response to surfactant stress. In this study, we demonstrate that the SiaABC proteins represent a signal response pathway that functions through a partner switch mechanism to control biofilm formation. We also demonstrate that SiaABCD functionality is dependent on carbon substrate availability for a variety of substrates, and that upon carbon starvation, SiaB mutants show impaired dispersal, in particular with the primary fermentation product ethanol. This suggests that carbon availability is at least one of the key environmental cues integrated by the SiaABCD system. Further, our biochemical, physiological and crystallographic data reveals that the phosphatase SiaA and its kinase counterpart SiaB balance the phosphorylation status of their target protein SiaC at threonine 68 (T68). Crystallographic analysis of the SiaA-PP2C domain shows that SiaA is present as a dimer. Dynamic modelling of SiaA with SiaC suggested that SiaA interacts strongly with phosphorylated SiaC and dissociates rapidly upon dephosphorylation of SiaC. Further, we show that the known phosphatase inhibitor fumonisin inhibits SiaA mediated phosphatase activity in vitro. In conclusion, the present work improves our understanding of how P. aeuruginosa integrates specific environmental conditions, such as carbon availability and surfactant stress, to regulate cellular aggregation and biofilm formation. With the biochemical and structural characterization of SiaA, initial data on the catalytic inhibition of SiaA, and the interaction between SiaA and SiaC, our study identifies promising targets for the development of biofilm-interference drugs to combat infections of this aggressive opportunistic pathogen.

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11

Mei, Y., C. Xie, W. Xie, Z. Wu, and M. Wu. "Siah-1S, a novel splice variant of Siah-1 (seven in absentia homolog), counteracts Siah-1-mediated downregulation of β-catenin." Oncogene 26, no. 43 (April 9, 2007): 6319–31. http://dx.doi.org/10.1038/sj.onc.1210449.

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12

Abada, Rinat, Tsofia Dreyfuss-Grossman, Yifat Herman-Bachinsky, Haim Geva, Shiri-Rivka Masa, and Ronit Sarid. "SIAH-1 Interacts with the Kaposi's Sarcoma-Associated Herpesvirus-Encoded ORF45 Protein and Promotes Its Ubiquitylation and Proteasomal Degradation." Journal of Virology 82, no. 5 (December 12, 2007): 2230–40. http://dx.doi.org/10.1128/jvi.02285-07.

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ABSTRACT Kaposi's sarcoma-associated herpesvirus (KSHV), also referred to as human herpesvirus 8, is a potentially tumorigenic virus implicated in the etiology of Kaposi's sarcoma, primary effusion lymphoma, and some forms of multicentric Castleman's disease. The open reading frame 45 (ORF45) protein, encoded by the KSHV genome, is capable of inhibiting virus-dependent interferon induction and appears to be essential for both early and late stages of infection. In the present study, we show, both in yeast two-hybrid assays and in mammalian cells, that the ORF45 protein interacts with the cellular ubiquitin E3 ligase family designated seven in absentia homologue (SIAH). We provide evidence that SIAH-1 promotes the degradation of KSHV ORF45 through a RING domain-dependent mechanism and via the ubiquitin-proteasome system. Furthermore, our data indicate the involvement of SIAH-1 in the regulation of the expression of ORF45 in KSHV-infected cells. Since the availability of KSHV ORF45 is expected to influence the course of KSHV infection, our findings identify a novel biological role for SIAH proteins as modulators of virus infection.

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13

Wong, Christina S. F., and Andreas Möller. "Siah: A Promising Anticancer Target." Cancer Research 73, no. 8 (March 1, 2013): 2400–2406. http://dx.doi.org/10.1158/0008-5472.can-12-4348.

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14

Reed, John C., and Kathryn R. Ely. "Degrading liaisons: Siah structure revealed." Nature Structural Biology 9, no. 1 (January 1, 2002): 8–10. http://dx.doi.org/10.1038/nsb0102-8.

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15

Matsuzawa, Shu-ichi, Chenglong Li, Chao-Zhou Ni, Shinichi Takayama, John C. Reed, and Kathryn R. Ely. "Structural Analysis of Siah1 and Its Interactions with Siah-interacting Protein (SIP)." Journal of Biological Chemistry 278, no. 3 (November 5, 2002): 1837–40. http://dx.doi.org/10.1074/jbc.m210263200.

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16

Sourisseau, T., C. Desbois, L. Debure, D. D. Bowtell, A. C. Cato, J. Schneikert, E. Moyse, and D. Michel. "Alteration of the stability of Bag-1 protein in the control of olfactory neuronal apoptosis." Journal of Cell Science 114, no. 7 (April 1, 2001): 1409–16. http://dx.doi.org/10.1242/jcs.114.7.1409.

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Normal apoptosis occurs continuously in the olfactory neuroepithelium of adult vertebrates, making it a useful model for studying neuronal apoptosis. Here we demonstrate that overexpression of the anti-apoptotic Bag-1 gene in olfactory neuronal cells confers a strong resistance to apoptosis. Conversely decreased levels of Bag-1 were found to precede a massive wave of olfactory neuronal apoptosis triggered by synaptic target ablation. We show that the decrease is brought about by ubiquitination and subsequent degradation of the Bag-1 protein. The ring finger protein Siah-2 is a likely candidate for the ubiquitination reaction since Siah-2 mRNA accumulated in lesioned olfactory neuroepithelium and overexpression of Siah-2 stimulated Bag-1 ubiquitination and degradation in transient expression assays. These results together identify destabilization of Bag-1 as a necessary step in olfactory neuronal apoptosis.

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17

Lou, Kai-Jye. "A SIAH of K-RAS relief." Science-Business eXchange 1, no. 44 (December 2008): 1063. http://dx.doi.org/10.1038/scibx.2008.1063.

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18

Lyons, Lisa. ""The Poetry Garden" by Siah Armajani." Design Quarterly, no. 160 (1994): 8. http://dx.doi.org/10.2307/4091322.

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19

Möller, A., C. M. House, C. S. F. Wong, D. B. Scanlon, M. C. P. Liu, Z. Ronai, and D. D. L. Bowtell. "Inhibition of Siah ubiquitin ligase function." Oncogene 28, no. 2 (October 13, 2008): 289–96. http://dx.doi.org/10.1038/onc.2008.382.

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20

Krämer, O. H., R. H. Stauber, G. Bug, J. Hartkamp, and S. K. Knauer. "SIAH proteins: critical roles in leukemogenesis." Leukemia 27, no. 4 (October 5, 2012): 792–802. http://dx.doi.org/10.1038/leu.2012.284.

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21

Jokar, Ali, Hamid Zare, Abdolrasool Zakerin, and Abdolhossein Aboutalebi Jahromi. "Effects of Shade Net Colors on Mineral Elements and Postharvest Shelf Life and Quality of Fresh Fig (Ficus carica L.) under Rain-Fed Condition." Horticulturae 7, no. 5 (May 1, 2021): 93. http://dx.doi.org/10.3390/horticulturae7050093.

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Photoselective netting is well known for filtering the intercepted solar radiation, thus affecting light quality. While its effects on leaf mineral elements have been well investigated, how color netting affects fruit mineral nutrients remains elusive. This study was conducted to evaluate the effects of shade provided by blue and yellow nets on mineral nutrients of fig trees under rain-fed conditions. The experiment was arranged as a split-plot treatment in a randomized complete block design with three replications. Cultivars “Sabz” and “Siah” were covered with color nets or left uncovered (as the control group). The highest nitrogen content (8710 ppm) was recorded for cultivar “Sabz” covered with blue net. Color nets enhanced calcium concentration in cultivar “Siah”. Covering fig trees with yellow net increased magnesium content in cultivar “Siah” and phosphorus content in cultivar “Sabz”. Our observation showed the significant positive effect of photo selective nets on postharvest quality, by decreasing fig fruit weight loss and extending shelf life of fruits. In general, color nets as a new agro-technological approach can maintain fruit nutrition under rain-fed conditions and increase postharvest shelf life and quality of fresh fig.

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22

Qi, Jianfei, Hyungsoo Kim, Marzia Scortegagna, and Ze’ev A. Ronai. "Regulators and Effectors of Siah Ubiquitin Ligases." Cell Biochemistry and Biophysics 67, no. 1 (May 23, 2013): 15–24. http://dx.doi.org/10.1007/s12013-013-9636-2.

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23

House, C. M., I. J. Frew, H. L. Huang, G. Wiche, N. Traficante, E. Nice, B. Catimel, and D. D. L. Bowtell. "A binding motif for Siah ubiquitin ligase." Proceedings of the National Academy of Sciences 100, no. 6 (March 7, 2003): 3101–6. http://dx.doi.org/10.1073/pnas.0534783100.

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24

Stebbins, John L., Eugenio Santelli, Yongmei Feng, Surya K. De, Angela Purves, Khatereh Motamedchaboki, Bainan Wu, Ze’ev A. Ronai, Robert C. Liddington, and Maurizio Pellecchia. "Structure-Based Design of Covalent Siah Inhibitors." Chemistry & Biology 20, no. 8 (August 2013): 973–82. http://dx.doi.org/10.1016/j.chembiol.2013.06.008.

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25

Gupta, Gagan K., Amber L. Collier, Dasom Lee, Richard A. Hoefer, Vasilena Zheleva, Lauren L. Siewertsz van Reesema, Angela M. Tang-Tan, et al. "Perspectives on Triple-Negative Breast Cancer: Current Treatment Strategies, Unmet Needs, and Potential Targets for Future Therapies." Cancers 12, no. 9 (August 24, 2020): 2392. http://dx.doi.org/10.3390/cancers12092392.

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Triple-negative breast cancer (TNBC), characterized by the absence or low expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor (HER2), is the most aggressive subtype of breast cancer. TNBC accounts for about 15% of breast cancer cases in the U.S., and is known for high relapse rates and poor overall survival (OS). Chemo-resistant TNBC is a genetically diverse, highly heterogeneous, and rapidly evolving disease that challenges our ability to individualize treatment for incomplete responders and relapsed patients. Currently, the frontline standard chemotherapy, composed of anthracyclines, alkylating agents, and taxanes, is commonly used to treat high-risk and locally advanced TNBC. Several FDA-approved drugs that target programmed cell death protein-1 (Keytruda) and programmed death ligand-1 (Tecentriq), poly ADP-ribose polymerase (PARP), and/or antibody drug conjugates (Trodelvy) have shown promise in improving clinical outcomes for a subset of TNBC. These inhibitors that target key genetic mutations and specific molecular signaling pathways that drive malignant tumor growth have been used as single agents and/or in combination with standard chemotherapy regimens. Here, we review the current TNBC treatment options, unmet clinical needs, and actionable drug targets, including epidermal growth factor (EGFR), vascular endothelial growth factor (VEGF), androgen receptor (AR), estrogen receptor beta (ERβ), phosphoinositide-3 kinase (PI3K), mammalian target of rapamycin (mTOR), and protein kinase B (PKB or AKT) activation in TNBC. Supported by strong evidence in developmental, evolutionary, and cancer biology, we propose that the K-RAS/SIAH pathway activation is a major tumor driver, and SIAH is a new drug target, a therapy-responsive prognostic biomarker, and a major tumor vulnerability in TNBC. Since persistent K-RAS/SIAH/EGFR pathway activation endows TNBC tumor cells with chemo-resistance, aggressive dissemination, and early relapse, we hope to design an anti-SIAH-centered anti-K-RAS/EGFR targeted therapy as a novel therapeutic strategy to control and eradicate incurable TNBC in the future.

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López Santana, Pablo. "SIAH DAREH. TERRAZAS Y PAISAJE EN ABBAS KIAROSTAMI." Proyecto, Progreso, Arquitectura, no. 21 (2019): 87–100. http://dx.doi.org/10.12795/ppa.2019.i21.06.

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27

Maeda, Ayaka, Tatsushi Yoshida, Katsuyuki Kusuzaki, and Toshiyuki Sakai. "The characterization of the human Siah-1 promoter1." FEBS Letters 512, no. 1-3 (January 18, 2002): 223–26. http://dx.doi.org/10.1016/s0014-5793(02)02265-2.

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28

Ren, Dong, Yuhu Dai, Qing Yang, Xin Zhang, Wei Guo, Liping Ye, Shuai Huang, et al. "Wnt5a induces and maintains prostate cancer cells dormancy in bone." Journal of Experimental Medicine 216, no. 2 (December 28, 2018): 428–49. http://dx.doi.org/10.1084/jem.20180661.

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In a substantial fraction of prostate cancer (PCa) patients, bone metastasis appears after years or even decades of latency. Canonical Wnt/β-catenin signaling has been proposed to be implicated in dormancy of cancer cells. However, how these tumor cells are kept dormant and recur under control of Wnt/β-catenin signaling derived from bone microenvironment remains unknown. Here, we report that Wnt5a from osteoblastic niche induces dormancy of PCa cells in a reversible manner in vitro and in vivo via inducing Siah E3 Ubiquitin Protein Ligase 2 (SIAH2) expression, which represses Wnt/β-catenin signaling. Furthermore, this effect of Wnt5a-induced dormancy of PCa cells depends on receptor tyrosine kinase-like orphan receptor 2 (ROR2), and a negative correlation of ROR2 expression with bone metastasis–free survival is observed in PCa patients. Therefore, these results demonstrate that Wnt5a/ROR2/SIAH2 signaling axis plays a crucial role in inducing and maintaining PCa cells dormancy in bone, suggesting a potential therapeutic utility of Wnt5a via inducing dormancy of PCa cells in bone.

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29

Fiucci, G., S. Beaucourt, D. Duflaut, A. Lespagnol, P. Stumptner-Cuvelette, A. Geant, G. Buchwalter, et al. "Siah-1b is a direct transcriptional target of p53: Identification of the functional p53 responsive element in the siah-1b promoter." Proceedings of the National Academy of Sciences 101, no. 10 (February 25, 2004): 3510–15. http://dx.doi.org/10.1073/pnas.0400177101.

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30

Park, Tae-Ju, Hiroki Hamanaka, Toshio Ohshima, Noriko Watanabe, Katsuhiko Mikoshiba, and Nobuyuki Nukina. "Inhibition of ubiquitin ligase Siah-1A by disabled-1." Biochemical and Biophysical Research Communications 302, no. 4 (March 2003): 671–78. http://dx.doi.org/10.1016/s0006-291x(03)00247-x.

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31

Beeson, Simon. "Material Thought: Siah Armajani and the Half-Open Door." Architecture and Culture 4, no. 3 (September 2016): 511–17. http://dx.doi.org/10.1080/20507828.2016.1239944.

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32

Boehm, J. "Regulation of BOB.1/OBF.1 stability by SIAH." EMBO Journal 20, no. 15 (August 1, 2001): 4153–62. http://dx.doi.org/10.1093/emboj/20.15.4153.

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33

Nagano, Yoshito, Hiroshi Yamashita, Tetsuya Takahashi, Shosei Kishida, Takeshi Nakamura, Eizo Iseki, Nobutaka Hattori, Yoshikuni Mizuno, Akira Kikuchi, and Masayasu Matsumoto. "Siah-1 Facilitates Ubiquitination and Degradation of Synphilin-1." Journal of Biological Chemistry 278, no. 51 (September 23, 2003): 51504–14. http://dx.doi.org/10.1074/jbc.m306347200.

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Nakayama, Koh, and Ze’ev Ronai. "Siah: New Players in the Cellular Response to Hypoxia." Cell Cycle 3, no. 11 (November 3, 2004): 1345–47. http://dx.doi.org/10.4161/cc.3.11.1207.

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Susini, L., B. J. Passer, N. Amzallag-Elbaz, T. Juven-Gershon, S. Prieur, N. Privat, M. Tuynder, et al. "Siah-1 binds and regulates the function of Numb." Proceedings of the National Academy of Sciences 98, no. 26 (December 18, 2001): 15067–72. http://dx.doi.org/10.1073/pnas.261571998.

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Hara, Makoto R., and Solomon H. Snyder. "Nitric Oxide–GAPDH–Siah: A Novel Cell Death Cascade." Cellular and Molecular Neurobiology 26, no. 4-6 (April 22, 2006): 525–36. http://dx.doi.org/10.1007/s10571-006-9011-6.

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Widhiantara, I. Gede, Anak Agung Ayu Putri Permatasari, I. Wayan Rosiana, I. Wayan Putu Sutirtayasa, and Ferbian Milas Siswanto. "Role of HIF-1, Siah-1 and SKN-1 in Inducing Adiposity for Caenorhabditis elegans under Hypoxic Conditions." Indonesian Biomedical Journal 12, no. 1 (March 19, 2020): 51–6. http://dx.doi.org/10.18585/inabj.v12i1.1007.

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Abstract:

BACKGROUND: Hypoxia has been shown to be able to induce adiposity. However, the mechanism and factors involved in this effect still remains unclear. Hence, we sought to investigate the role of oxygensensitive factors regarding hypoxia-induced adiposity in nematode Caenorhabditis elegans.METHODS: The C. elegans were grown on nematode growth medium (NGM) agar plates seeded with Escherichia coli OP50 at 20°C. The ratio of width/body length was measured using the morphometry analysis. Fat accumulation was examined using Sudan Black methods. Protein levels of sterol binding protein (SBP)-1 were assessed by immunoblotting. Lifespan assay was performed at 20°C and was monitored every two days.RESULTS: The results showed that of all mutant used, only hif-1 mutant which did not experience an increase in the ratio of width/body length (p>0.05) and fat accumulation (p>0.05), indicating that hypoxia-inducible factors (HIF)-1 plays an important role in the pathogenesis of hypoxia-induced adiposity. Both siah-1 and skn-1 mutants experienced SBP-1 protein elevation (p<0.05), and increased fat-6 mRNA expression (p<0.05) which were not experienced by a hif-1 mutant (p>0.05) further supporting that HIF-1 acts as an upstream regulator fromSBP-1.CONCLUSION: In general, the results of this study provide evidences of the involvement of the transcription factor HIF-1 in inducing adiposity under the hypoxic conditions. However, we did not find the involvement of seven in absentia homolog-1 (Siah-1) and skinhead-1 (SKN-1).KEYWORDS: hypoxia, adiposity, fat, HIF-1, Siah-1, SKN-1, C. elegans

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Iwai, Akio, Hiroyuki Marusawa, Shu-ichi Matsuzawa, Toru Fukushima, Makoto Hijikata, John C. Reed, Kunitada Shimotohno, and Tsutomu Chiba. "Siah-1L, a novel transcript variant belonging to the human Siah family of proteins, regulates β-catenin activity in a p53-dependent manner." Oncogene 23, no. 45 (August 23, 2004): 7593–600. http://dx.doi.org/10.1038/sj.onc.1208016.

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Dickins, Ross A., Ian J. Frew, Colin M. House, Moira K. O'Bryan, Andrew J. Holloway, Izhak Haviv, Nadia Traficante, David M. de Kretser, and David D. L. Bowtell. "The Ubiquitin Ligase Component Siah1a Is Required for Completion of Meiosis I in Male Mice." Molecular and Cellular Biology 22, no. 7 (April 1, 2002): 2294–303. http://dx.doi.org/10.1128/mcb.22.7.2294-2303.2002.

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ABSTRACT The mammalian Siah genes encode highly conserved proteins containing a RING domain. As components of E3 ubiquitin ligase complexes, Siah proteins facilitate the ubiquitination and degradation of diverse protein partners including β-catenin, N-CoR, and DCC. We used gene targeting in mice to analyze the function of Siah1a during mammalian development and reveal novel roles in growth, viability, and fertility. Mutant animals have normal weights at term but are postnatally growth retarded, despite normal levels of pituitary growth hormone. Embryonic fibroblasts isolated from mutant animals grow normally. Most animals die before weaning, and few survive beyond 3 months. Serum gonadotropin levels are normal in Siah1a mutant mice; however, females are subfertile and males are sterile due to a block in spermatogenesis. Although spermatocytes in mutant mice display normal meiotic prophase and meiosis I spindle formation, they accumulate at metaphase to telophase of meiosis I and subsequently undergo apoptosis. The requirement of Siah1a for normal progression beyond metaphase I suggests that Siah1a may be part of a novel E3 complex acting late in the first meiotic division.

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House, Colin M., Nancy C. Hancock, Andreas Möller, Brett A. Cromer, Victor Fedorov, David D. L. Bowtell, Michael W. Parker, and Galina Polekhina. "Elucidation of the Substrate Binding Site of Siah Ubiquitin Ligase." Structure 14, no. 4 (April 2006): 695–701. http://dx.doi.org/10.1016/j.str.2005.12.013.

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Garrison, Jason B., Ricardo G. Correa, Motti Gerlic, Kenneth W. Yip, Andreas Krieg, Craig M. Tamble, Ranxin Shi, et al. "ARTS and Siah Collaborate in a Pathway for XIAP Degradation." Molecular Cell 41, no. 1 (January 2011): 107–16. http://dx.doi.org/10.1016/j.molcel.2010.12.002.

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Kang, Nami, Minho Won, Myungchull Rhee, and Hyunju Ro. "Siah Ubiquitin Ligases Modulate Nodal Signaling during Zebrafish Embryonic Development." Molecules and Cells 37, no. 5 (May 2014): 389–98. http://dx.doi.org/10.14348/molcells.2014.0032.

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Cooper, Sarah E. "In vivo function of a novel Siah protein in Drosophila." Mechanisms of Development 124, no. 7-8 (August 2007): 584–91. http://dx.doi.org/10.1016/j.mod.2007.04.007.

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Bruzzoni-Giovanelli, H., A. Faille, G. Linares-Cruz, M. Nemani, F. Le Deist, A. Germani, D. Chassoux, et al. "SIAH-1 inhibits cell growth by altering the mitotic process." Oncogene 18, no. 50 (November 1999): 7101–9. http://dx.doi.org/10.1038/sj.onc.1203187.

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Kim, Chang Jae, Yong Gu Cho, Cho Hyun Park, Seong Whan Jeong, Suk Woo Nam, Su Young Kim, Sug Hyung Lee, Nam Jin Yoo, Jung Young Lee, and Won Sang Park. "Inactivating mutations of the Siah-1 gene in gastric cancer." Oncogene 23, no. 53 (October 4, 2004): 8591–96. http://dx.doi.org/10.1038/sj.onc.1208113.

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Casad, Michelle E., Lin Yu, Joseph P. Daniels, Matthew J. Wolf, and Howard A. Rockman. "Deletion of Siah-interacting protein gene in Drosophila causes cardiomyopathy." Molecular Genetics and Genomics 287, no. 4 (March 8, 2012): 351–60. http://dx.doi.org/10.1007/s00438-012-0684-x.

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Piedade, Warlen Pereira, and Jakub K. Famulski. "E3 ubiquitin ligase-mediated regulation of vertebrate ocular development; new insights into the function of SIAH enzymes." Biochemical Society Transactions 49, no. 1 (February 22, 2021): 327–40. http://dx.doi.org/10.1042/bst20200613.

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Developmental regulation of the vertebrate visual system has been a focus of investigation for generations as understanding this critical time period has direct implications on our understanding of congenital blinding disease. The majority of studies to date have focused on transcriptional regulation mediated by morphogen gradients and signaling pathways. However, recent studies of post translational regulation during ocular development have shed light on the role of the ubiquitin proteasome system (UPS). This rather ubiquitous yet highly diverse system is well known for regulating protein function and localization as well as stability via targeting for degradation by the 26S proteasome. Work from many model organisms has recently identified UPS activity during various milestones of ocular development including retinal morphogenesis, retinal ganglion cell function as well as photoreceptor homeostasis. In particular work from flies and zebrafish has highlighted the role of the E3 ligase enzyme family, Seven in Absentia Homologue (Siah) during these events. In this review, we summarize the current understanding of UPS activity during Drosophila and vertebrate ocular development, with a major focus on recent findings correlating Siah E3 ligase activity with two major developmental stages of vertebrate ocular development, retinal morphogenesis and photoreceptor specification and survival.

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Santelli, Eugenio, Marilisa Leone, Chenlong Li, Toru Fukushima, Nicholas E. Preece, Arthur J. Olson, Kathryn R. Ely, et al. "Structural Analysis of Siah1-Siah-interacting Protein Interactions and Insights into the Assembly of an E3 Ligase Multiprotein Complex." Journal of Biological Chemistry 280, no. 40 (August 4, 2005): 34278–87. http://dx.doi.org/10.1074/jbc.m506707200.

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Oliver, P. L., E. Bitoun, J. Clark, E. L. Jones, and K. E. Davies. "Mediation of Af4 protein function in the cerebellum by Siah proteins." Proceedings of the National Academy of Sciences 101, no. 41 (September 30, 2004): 14901–6. http://dx.doi.org/10.1073/pnas.0406196101.

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Ko, S. J., K. Isozaki, I. Kim, J. H. Lee, H. J. Cho, S. Y. Sohn, S. R. Oh, et al. "PKC Phosphorylation Regulates mGluR5 Trafficking by Enhancing Binding of Siah-1A." Journal of Neuroscience 32, no. 46 (November 14, 2012): 16391–401. http://dx.doi.org/10.1523/jneurosci.1964-12.2012.

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