Mice lacking the transcription factor Mist1 exhibit an altered stress response and increased sensitivity to caerulein-induced pancreatitis. - Wikidata - awgldk - TriplyDB

Mice lacking the transcription factor Mist1 exhibit an altered stress response and increased sensitivity to caerulein-induced pancreatitis.

Mice lacking the transcription factor Mist1 exhibit an altered stress response and increased sensitivity to caerulein-induced pancreatitis.

http://www.wikidata.org/entity/Q53582791

about

RAB26 and RAB3D are direct transcriptional targets of MIST1 that regulate exocrine granule maturation Silencing Mist1 Gene Expression Is Essential for Recovery from Acute Pancreatitis Epigenetic reprogramming in Mist1(-/-) mice predicts the molecular response to cerulein-induced pancreatitis The absence of MIST1 leads to increased ethanol sensitivity and decreased activity of the unfolded protein response in mouse pancreatic acinar cells Quantitative organellar proteomics analysis of rough endoplasmic reticulum from normal and acute pancreatitis rat pancreas RAB26 coordinates lysosome traffic and mitochondrial localization.Characterization of 5-(2- 18F-fluoroethoxy)-L-tryptophan for PET imaging of the pancreas.Identification of key transcription factors in caerulein-induced pancreatitis through expression profiling data.Loss of the acinar-restricted transcription factor Mist1 accelerates Kras-induced pancreatic intraepithelial neoplasia.Mist1 regulates pancreatic acinar cell proliferation through p21 CIP1/WAF1 Stanniocalcin 2 alters PERK signalling and reduces cellular injury during cerulein induced pancreatitis in mice.Transcription factor MIST1 in terminal differentiation of mouse and human plasma cells.Regeneration and repair of the exocrine pancreas.MIST1 regulates the pancreatic acinar cell expression of Atp2c2, the gene encoding secretory pathway calcium ATPase 2.Induced Mist1 expression promotes remodeling of mouse pancreatic acinar cells Scaling factors: transcription factors regulating subcellular domains.Endoplasmic reticulum stress and the pancreatic acinar cell.MIST1 Links Secretion and Stress as Both Target and Regulator of the UPR.MIST1 and PTF1 Collaborate in Feed-forward Regulatory Loops that Maintain the Pancreatic Acinar Phenotype in Adult Mice.Pathogenesis of pancreatic cancer: lessons from animal models.PAR2 regulates regeneration, transdifferentiation, and death Globally increased ultraconserved noncoding RNA expression in pancreatic adenocarcinoma.Acinar cell reprogramming: a clinically important target in pancreatic disease.Extensive pancreas regeneration following acinar-specific disruption of Xbp1 in mice.Endoplasmic reticulum stress is activated in acute pancreatitis.Acinar cell plasticity and development of pancreatic ductal adenocarcinoma.Maintenance of acinar cell organization is critical to preventing Kras-induced acinar-ductal metaplasia.A soluble form of human nectin-2 impairs exocrine secretion of pancreas and formation of zymogen granules in transgenic mice Atp2c2 Is Transcribed From a Unique Transcriptional Start Site in Mouse Pancreatic Acinar Cells.Silencing of the Fibroblast growth factor 21 gene is an underlying cause of acinar cell injury in mice lacking MIST1.Glucagon-like peptide-1 receptor activation modulates pancreatitis-associated gene expression but does not modify the susceptibility to experimental pancreatitis in mice.Pancreas-specific aquaporin 12 null mice showed increased susceptibility to caerulein-induced acute pancreatitis.Activating transcription factor 3 promotes loss of the acinar cell phenotype in response to cerulein-induced pancreatitis in mice.Resveratrol Ameliorates the Severity of Fibrogenesis in Mice with Experimental Chronic Pancreatitis.Maturity and age influence chief cell ability to transdifferentiate into metaplasia.p21(WAF1) (/Cip1) limits senescence and acinar-to-ductal metaplasia formation during pancreatitis.Activation of protein kinase Cδ leads to increased pancreatic acinar cell dedifferentiation in the absence of MIST1.

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P2860

Mice lacking the transcription factor Mist1 exhibit an altered stress response and increased sensitivity to caerulein-induced pancreatitis.

http://www.wikidata.org/entity/Q53582791

description

2006 nî lūn-bûn

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2006年の論文

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年學術文章

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2006年學術文章

@zh-hant

name

Mice lacking the transcription ...... aerulein-induced pancreatitis.

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Mice lacking the transcription ...... aerulein-induced pancreatitis.

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type

label

Mice lacking the transcription ...... aerulein-induced pancreatitis.

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Mice lacking the transcription ...... aerulein-induced pancreatitis.

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Mice lacking the transcription ...... aerulein-induced pancreatitis.

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Mice lacking the transcription ...... aerulein-induced pancreatitis.

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P356

AJPGI.00512.2006

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American Journal of Physiology - Gastrointestinal and Liver Physiology

P1476

Mice lacking the transcription ...... aerulein-induced pancreatitis.

@en

P2093

Agnes S Kowalik

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Charis L Johnson

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Christopher L Pin

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Elena N Fazio

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Jacqueline Y Weston

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Sami A Chadi

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P2860

ATF6 as a transcription activator of the endoplasmic reticulum stress element: thapsigargin stress-induced changes and synergistic interactions with NF-Y and YY1

ASK1 is essential for endoplasmic reticulum stress-induced neuronal cell death triggered by expanded polyglutamine repeats

Control of PERK eIF2alpha kinase activity by the endoplasmic reticulum stress-induced molecular chaperone P58IPK.

The bHLH transcription factor Mist1 is required to maintain exocrine pancreas cell organization and acinar cell identity

Perk is essential for translational regulation and cell survival during the unfolded protein response

Mutations of the cationic trypsinogen gene in hereditary and non-hereditary pancreatitis

ER Ca2+ depletion triggers apoptotic signals for endoplasmic reticulum (ER) overload response induced by overexpressed reticulon 3 (RTN3/HAP)

Protein translation and folding are coupled by an endoplasmic-reticulum-resident kinase

Activating transcription factor 3 is integral to the eukaryotic initiation factor 2 kinase stress response

Feedback inhibition of the unfolded protein response by GADD34-mediated dephosphorylation of eIF2alpha

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10.1152/AJPGI.00512.2006

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4

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292

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17170023

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