ArticleBioinformation2013
Novel genes underlying beta cell survival in metabolic stress.
Article in Bioinformation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Identification of direct transcriptional targets of NFATC2 that promote β cell proliferation.The Journal of clinical investigation · 2021Article
- The dual role of BI 2536, a small-molecule inhibitor that targets PLK1, in induction of apoptosis and attenuation of autophagy in neuroblastoma cells.Journal of Cancer · 2020Article
- Gene expression profiling of periodontitis-affected gingival tissue by spatial transcriptomics.Scientific reports · 2018Article
- Genetic causes of hypomagnesemia, a clinical overview.Pediatric nephrology (Berlin, Germany) · 2017Review
- GIT2 Acts as a Systems-Level Coordinator of Neurometabolic Activity and Pathophysiological Aging.Frontiers in endocrinology · 2015Article
- Commentary: "prom1 function in development, intestinal inflammation, and intestinal tumorigenesis".Frontiers in oncology · 2015Article
- Article
- A new congenital disorder of glycosylation caused by a mutation in SSR4, the signal sequence receptor 4 protein of the TRAP complex.Human molecular genetics · 2014Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Relative insulin deficiency, in response to increased metabolic demand (obesity, genetic insulin resistance, pregnancy and aging) lead to Type2 diabetes. Susceptibility of the type 2 diabetes has a genetic basis, as a subset of people with risk factors (obesity, Insulin Resistance, pregnancy), develop Type2 Diabetes. We aimed to identify 'cluster' of overexpressed genes, underlying increased beta cell survival in diabetes resistant C57BL/6J ob/ob mice (compared to diabetes susceptible BTBR ob/ob mice). We used 'consensus' overexpression status to identify 'cluster' of 11 genes consisting of Aldh18a1, Rfc4, Dynlt3, Prom1, H13, Psen1, Ssr4, Dad1, Anpep, Fam111a and Plk1. Information (biological processes, molecular functions, cellular components, protein-protein interactions/associations, gene deletion/knockout/inhibition studies) of all the genes in 'cluster' were collected by text mining using different literature search tools, gene information databases and protein-protein interaction databases. Beta cell specific function of these genes were also inferred using meta analysis tool of Beta Cell Biology Consortium, by studying the expression pattern of these genes in microarray studies related to beta-cell stimulation/injury, pancreas development and growth and cell differentiation. In the 'clusters', 6 genes (Dad1, Psen1, Ssr4, Rfc4, H13, Plk1) have a role in cell survival. Only Psen1 was previously identified to have role in successful beta cell compensation. We advocate these genes to be potentially involved in successful beta cell compensation and prevent T2D in humans, by conferring protection against diabetogenic insults.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.