Difference between revisions of "OXCT1-AS1"
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The anti-apoptotic evolutionary conserved lncRNA OXCT1-AS1 as a regulator of cardiomyocyte survival.<ref name="ref2" /> | The anti-apoptotic evolutionary conserved lncRNA OXCT1-AS1 as a regulator of cardiomyocyte survival.<ref name="ref2" /> | ||
===Regulation=== | ===Regulation=== | ||
| − | [[File: OXCT1-AS1. | + | [[File: OXCT1-AS1.jpeg|thumb|300px|OXCT1-AS1 activates gene expression via triple helix formation with gene promoters.<ref name="ref2"/>]] |
OXCT1-AS1 inhibited miR-455-5p to decrease its binding to the JAK1 3'-untranslated region, which could upregulate the expression of JAK1 at the protein level, thus promoting BCa proliferation and invasion.<ref name="ref1" /> | OXCT1-AS1 inhibited miR-455-5p to decrease its binding to the JAK1 3'-untranslated region, which could upregulate the expression of JAK1 at the protein level, thus promoting BCa proliferation and invasion.<ref name="ref1" /> | ||
| − | OXCT1-AS1 directly binds to the promoters of genes downregulated after OXCT1-AS1 silencing via RNA-DNA triple helix formation and cardiomyocytes lacking the triple helix forming domain of OXCT1-AS1 show an increase in apoptosis.<ref name="ref2" /> | + | OXCT1-AS1 directly binds to the promoters of genes downregulated after OXCT1-AS1 silencing via RNA-DNA triple helix formation and cardiomyocytes lacking the triple helix forming domain of OXCT1-AS1 show an increase in apoptosis.<ref name="ref2" /> |
| + | |||
===Expression=== | ===Expression=== | ||
One of the direct OXCT1-AS1 targets is NRF2, and restoration of NRF2 levels after SARRAH silencing partially rescues the reduction in cell viability.<ref name="ref2" /> | One of the direct OXCT1-AS1 targets is NRF2, and restoration of NRF2 levels after SARRAH silencing partially rescues the reduction in cell viability.<ref name="ref2" /> | ||
Revision as of 01:59, 19 February 2021
LncRNA OXCT1-AS1 as the aging-regulated lncRNA Sarrah that is anti-apoptotic in cardiomyocytes and can upregulate the expression of JAK1 at the protein level promoting BCa proliferation and invasion.[1] [2]
Contents
Annotated Information
Name
Approved symbol:OXCT1-AS1
Approved name:OXCT1 antisense RNA 1
HGNC ID HGNC:40423
Previous name:OXCT1 antisense RNA 1 (non-protein coding)
Alias symbol:SARRAH
RefSeq ID:NR_046635
LncBook ID:HSALNG0041428|HSALNG0041428|HSALNG0041428
Characteristics
Please input information here.
Function
OXCT1-AS1 perform a vital function in the pathogenesis and progression of BCa.[1] The anti-apoptotic evolutionary conserved lncRNA OXCT1-AS1 as a regulator of cardiomyocyte survival.[2]
Regulation
OXCT1-AS1 activates gene expression via triple helix formation with gene promoters.[2]
OXCT1-AS1 inhibited miR-455-5p to decrease its binding to the JAK1 3'-untranslated region, which could upregulate the expression of JAK1 at the protein level, thus promoting BCa proliferation and invasion.[1] OXCT1-AS1 directly binds to the promoters of genes downregulated after OXCT1-AS1 silencing via RNA-DNA triple helix formation and cardiomyocytes lacking the triple helix forming domain of OXCT1-AS1 show an increase in apoptosis.[2]
Expression
One of the direct OXCT1-AS1 targets is NRF2, and restoration of NRF2 levels after SARRAH silencing partially rescues the reduction in cell viability.[2]
Diseases
Bladder cancer(BCa)[1] Cardiovascular disease[2]
Labs working on this lncRNA
- Department of Urology, Xiangya Hospital, Central South University,Changsha,China.[1]
- Institute for Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt am Main, Frankfurt am Main, Germany.[2]
- German Center for Cardiovascular Research (DZHK), Berlin, Germany.[2]
- Department of Physiology, VU University Medical Center, Amsterdam, the Netherlands.[2]
- Institute for Computational Genomics, Joint Research Center for Computational Biomedicine, RWTH Aachen University, Aachen, Germany.[2]
- Institute for Cardiovascular Physiology, Medical Faculty, Goethe University Frankfurt am Main, Frankfurt am Main, Germany.[2]
- Georg Speyer Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany.[2]
- Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.[2]
- Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, USA. [2]
- Department of Chemistry, Georgia State University, Atlanta, USA.[2]
- Institute of Biochemistry II, Goethe University, Frankfurt am Main, Germany.[2]
- Institute of Pharmacology and Toxicology, Technical University Munich, Munich, Germany.[2]
- Department of Nephrology, Technical University of Munich, School of Medicine, Klinikum rechts der Isar, Munich, Germany.[2]
- Department of Experimental Pharmacology and Toxicology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.[2]
- Functional Proteomics, Medical School, Goethe University Frankfurt am Main, Frankfurt am Main, Germany.[2]
- Department of Cardiovascular Physiology, Ruhr University Bochum, Bochum, Germany.[2]
- Laboratory Genetic Metabolic Diseases, Academic Medical Center, Amsterdam, the Netherlands.[2]
- Institute for Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt am Main, Frankfurt am Main, Germany. Boon@med.uni-frankfurt.de.[2]
- German Center for Cardiovascular Research (DZHK), Berlin, Germany. Boon@med.uni-frankfurt.de.[2]
- Department of Physiology, VU University Medical Center, Amsterdam, the Netherlands. Boon@med.uni-frankfurt.de.[2]
References
- ↑ 1.0 1.1 1.2 1.3 1.4 Chen JB, Zhu YW, Guo X, Yu C, Liu PH, Li C, Hu J, Li HH, Liu LF, Chen MF, Chen HQ, Xiong-Bing Z. Microarray expression profiles analysis revealed lncRNA OXCT1-AS1 promoted bladder cancer cell aggressiveness via miR-455-5p/JAK1 signaling. J Cell Physiol. 2019 Aug;234(8):13592-13601. doi: 10.1002/jcp.28037. Epub 2019 Jan 4.
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 2.22 2.23 2.24 Trembinski DJ, Bink DI, Theodorou K, Sommer J, Fischer A, van Bergen A, Kuo CC, Costa IG, Schürmann C, Leisegang MS, Brandes RP, Alekseeva T, Brill B, Wietelmann A, Johnson CN, Spring-Connell A, Kaulich M, Werfel S, Engelhardt S, Hirt MN, Yorgan K, Eschenhagen T, Kirchhof L, Hofmann P, Jaé N, Wittig I, Hamdani N, Bischof C, Krishnan J, Houtkooper RH, Dimmeler S, Boon RA. Aging-regulated anti-apoptotic long non-coding RNA Sarrah augments recovery from acute myocardial infarction. Nat Commun. 2020 Apr 27;11(1):2039. doi: 10.1038/s41467-020-15995-2.
