scholarly journals Ptf1a function and transcriptional cis‐regulation, a cornerstone in vertebrate pancreas development.

FEBS Journal ◽  
2021 ◽  
Author(s):  
Marta Duque ◽  
João Pedro Amorim ◽  
José Bessa
Keyword(s):  
Pancreas Development ◽  
Cis Regulation

Identification of MicroRNAs Regulating Ptf1a Expression in Mouse Pancreas Development*

2010 ◽  
Vol 2009 (12) ◽  
pp. 1607-1612
Author(s):  
Yang AN ◽  
Yan-Kun YANG ◽  
Fei GAO ◽  
Kuan-Yu ZHU ◽  
Tan-Wei MU ◽  
...  
Keyword(s):  
Pancreas Development ◽  
Mouse Pancreas

scholarly journals A pediatric brain tumor atlas of genes deregulated by somatic genomic rearrangement

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yiqun Zhang ◽  
Fengju Chen ◽  
Lawrence A. Donehower ◽  
Michael E. Scheurer ◽  
Chad J. Creighton
Keyword(s):  
Brain Tumor ◽  
Brain Tumors ◽  
Tyrosine Kinases ◽  
Pediatric Brain Tumor ◽  
Pediatric Brain Tumors ◽  
Altered Expression ◽  
Critical Pathways ◽  
Cis Regulation ◽  
Or Gene ◽  
Pediatric Brain

AbstractThe global impact of somatic structural variants (SSVs) on gene expression in pediatric brain tumors has not been thoroughly characterised. Here, using whole-genome and RNA sequencing from 854 tumors of more than 30 different types from the Children’s Brain Tumor Tissue Consortium, we report the altered expression of hundreds of genes in association with the presence of nearby SSV breakpoints. SSV-mediated expression changes involve gene fusions, altered cis-regulation, or gene disruption. SSVs considerably extend the numbers of patients with tumors somatically altered for critical pathways, including receptor tyrosine kinases (KRAS, MET, EGFR, NF1), Rb pathway (CDK4), TERT, MYC family (MYC, MYCN, MYB), and HIPPO (NF2). Compared to initial tumors, progressive or recurrent tumors involve a distinct set of SSV-gene associations. High overall SSV burden associates with TP53 mutations, histone H3.3 gene H3F3C mutations, and the transcription of DNA damage response genes. Compared to adult cancers, pediatric brain tumors would involve a different set of genes with SSV-altered cis-regulation. Our comprehensive and pan-histology genomic analyses reveal SSVs to play a major role in shaping the transcriptome of pediatric brain tumors.

scholarly journals NEUROD1 Is Required for the Early α and β Endocrine Differentiation in the Pancreas

2021 ◽  
Vol 22 (13) ◽  
pp. 6713
Author(s):  
Romana Bohuslavova ◽  
Ondrej Smolik ◽  
Jessica Malfatti ◽  
Zuzana Berkova ◽  
Zaneta Novakova ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Fate ◽  
Cell Mass ◽  
Neonatal Diabetes ◽  
Diabetes Research ◽  
Pancreas Development ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Islet Cell ◽  
Endocrine Differentiation

Diabetes is a metabolic disease that involves the death or dysfunction of the insulin-secreting β cells in the pancreas. Consequently, most diabetes research is aimed at understanding the molecular and cellular bases of pancreatic development, islet formation, β-cell survival, and insulin secretion. Complex interactions of signaling pathways and transcription factor networks regulate the specification, growth, and differentiation of cell types in the developing pancreas. Many of the same regulators continue to modulate gene expression and cell fate of the adult pancreas. The transcription factor NEUROD1 is essential for the maturation of β cells and the expansion of the pancreatic islet cell mass. Mutations of the Neurod1 gene cause diabetes in humans and mice. However, the different aspects of the requirement of NEUROD1 for pancreas development are not fully understood. In this study, we investigated the role of NEUROD1 during the primary and secondary transitions of mouse pancreas development. We determined that the elimination of Neurod1 impairs the expression of key transcription factors for α- and β-cell differentiation, β-cell proliferation, insulin production, and islets of Langerhans formation. These findings demonstrate that the Neurod1 deletion altered the properties of α and β endocrine cells, resulting in severe neonatal diabetes, and thus, NEUROD1 is required for proper activation of the transcriptional network and differentiation of functional α and β cells.

scholarly journals Cis-regulation of the L-type pyruvate kinase gene promoter by glucose, insulin and cyclic AMP

1992 ◽  
Vol 20 (8) ◽  
pp. 1871-1878 ◽  
Author(s):  
Marie-Odile Bergot ◽  
Maria-Jose M. Diaz-Guerra ◽  
Nathalie Puzenat ◽  
Michel Raymondjean ◽  
Axel Kahn
Keyword(s):  
Cyclic Amp ◽  
Pyruvate Kinase ◽  
Gene Promoter ◽  
Kinase Gene ◽  
Cis Regulation

scholarly journals Dissecting the Role of Glucocorticoids on Pancreas Development

Diabetes ◽  
2004 ◽  
Vol 53 (9) ◽  
pp. 2322-2329 ◽  
Author(s):  
E. Gesina ◽  
F. Tronche ◽  
P. Herrera ◽  
B. Duchene ◽  
W. Tales ◽  
...  
Keyword(s):  
Pancreas Development

scholarly journals MFng Is Dispensable for Mouse Pancreas Development and Function

2009 ◽  
Vol 29 (8) ◽  
pp. 2129-2138 ◽  
Author(s):  
Per Svensson ◽  
Ingela Bergqvist ◽  
Stefan Norlin ◽  
Helena Edlund
Keyword(s):  
Cell Differentiation ◽  
Notch Signaling ◽  
Pancreas Development ◽  
Loss Of Function ◽  
Pancreatic Cell ◽  
Targeted Deletion ◽  
Mouse Pancreas ◽  
Pancreatic Progenitor ◽  
Pancreatic Progenitor Cells ◽  
And Function

ABSTRACT Notch signaling regulates pancreatic cell differentiation, and mutations of various Notch signaling components result in perturbed pancreas development. Members of the Fringe family of β1,3-N-acetylglucosaminyltransferases, Manic Fringe (MFng), Lunatic Fringe (LFng), and Radical Fringe (RFng), modulate Notch signaling, and MFng has been suggested to regulate pancreatic endocrine cell differentiation. We have characterized the expression of the three mouse Fringe genes in the developing mouse pancreas between embryonic days 9 and 14 and show that the expression of MFng colocalized with the proendocrine transcription factor Ngn3. In contrast, the expression of LFng colocalized with the exocrine marker Ptf1a, whereas RFng was not expressed. Moreover, we show that expression of MFng is lost in Ngn3 mutant mice, providing evidence that MFng is genetically downstream of Ngn3. Gain- and loss-of-function analyses of MFng by the generation of mice that overexpress MFng in early pancreatic progenitor cells and mice with a targeted deletion of MFng provide, however, evidence that MFng is dispensable for pancreas development and function, since no pancreatic defects in these mice were observed.

scholarly journals Nom1 Mediates Pancreas Development by Regulating Ribosome Biogenesis in Zebrafish

PLoS ONE ◽  
2014 ◽  
Vol 9 (6) ◽  
pp. e100796 ◽  
Author(s):  
Wei Qin ◽  
Zelin Chen ◽  
Yihan Zhang ◽  
Ruibin Yan ◽  
Guanrong Yan ◽  
...  
Keyword(s):  
Ribosome Biogenesis ◽  
Pancreas Development

scholarly journals Combinatorial Cis-regulation in Saccharomyces Species

2016 ◽  
Vol 6 (3) ◽  
pp. 653-667 ◽  
Author(s):  
Aaron T. Spivak ◽  
Gary D. Stormo
Keyword(s):  
Cis Regulation
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