ArticleDiabetes2008
Postnatal expansion of the pancreatic beta-cell mass is dependent on survivin.
Article in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Review
- Milk Exosomal microRNAs: Postnatal Promoters of β Cell Proliferation but Potential Inducers of β Cell De-Differentiation in Adult Life.International journal of molecular sciences · 2022Review
- It's What and When You Eat: An Overview of Transcriptional and Epigenetic Responses to Dietary Perturbations in Pancreatic Islets.Frontiers in endocrinology · 2022Review
- Role and Significance of Circulating Biomarkers: miRNA and E2F1 mRNA Expression and Their Association with Type-2 Diabetic Complications.International journal of endocrinology · 2020Article
- Survivin expression pattern in the intestine of normoxic and ischemic rats.BMC gastroenterology · 2017Article
- Prolactin-stimulated survivin induction is required for beta cell mass expansion during pregnancy in mice.Diabetologia · 2015Article
- Review
- EGFR signaling promotes β-cell proliferation and survivin expression during pregnancy.PloS one · 2014Article
- Tcf19 is a novel islet factor necessary for proliferation and survival in the INS-1 β-cell line.American journal of physiology. Endocrinology and metabolism · 2013Article
- Genes involved in pancreatic islet cell rejuvenation.The Indian journal of medical research · 2013Review
- Rosiglitazone promotes PPARγ-dependent and -independent alterations in gene expression in mouse islets.Endocrinology · 2012Article
- Survivin is required for beta-cell mass expansion in the pancreatic duct-ligated mouse model.PloS one · 2012Article
- Acetylation directs survivin nuclear localization to repress STAT3 oncogenic activity.The Journal of biological chemistry · 2010Article
- Beta cell adaptation in pregnancy: a major difference between humans and rodents?Diabetologia · 2010Article
- EGF regulates survivin stability through the Raf-1/ERK pathway in insulin-secreting pancreatic β-cells.BMC molecular biology · 2010Article
- Gene expression profiles of Beta-cell enriched tissue obtained by laser capture microdissection from subjects with type 2 diabetes.PloS one · 2010Article
- Exocrine-to-endocrine differentiation is detectable only prior to birth in the uninjured mouse pancreas.BMC developmental biology · 2010Article
- Dimorphic histopathology of long-standing childhood-onset diabetes.Diabetologia · 2010Article
- Expansion of beta-cell mass in response to pregnancy.Trends in endocrinology and metabolism: TEM · 2010Review
- The transcriptional response of the islet to pregnancy in mice.Molecular endocrinology (Baltimore, Md.) · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 8 institutions in 1 country.
Funding
Abstract
objectiveDiabetes results from a deficiency of functional beta-cells due to both an increase in beta-cell death and an inhibition of beta-cell replication. The molecular mechanisms responsible for these effects in susceptible individuals are mostly unknown. The objective of this study was to determine whether a gene critical for cell division and cell survival in cancer cells, survivin, might also be important for beta-cells. RESEARCH DESIGN AND
methodsWe generated mice harboring a conditional deletion of survivin in pancreatic endocrine cells using mice with a Pax-6-Cre transgene promoter construct driving tissue-specific expression of Cre-recombinase in these cells. We performed metabolic studies and immunohistochemical analyses to determine the effects of a mono- and biallelic deletion of survivin.
resultsSelective deletion of survivin in pancreatic endocrine cells in the mouse had no discernible effects during embryogenesis but was associated with striking decreases in beta-cell number after birth, leading to hyperglycemia and early-onset diabetes by 4 weeks of age. Serum insulin levels were significantly decreased in animals lacking endocrine cell survivin, with relative stability of other hormones. Exogenous expression of survivin in mature beta-cells lacking endogenous survivin completely rescued the hyperglycemic phenotype and the decrease in beta-cell mass, confirming the specificity of the survivin effect in these cells.
conclusionsOur findings implicate survivin in the maintenance of beta-cell mass through both replication and antiapoptotic mechanisms. Given the widespread involvement of survivin in cancer, a novel role for survivin may well be exploited in beta-cell regulation in diseased states, such as diabetes.
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What OpenQuestion holds
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.