Nupr1 deletion protects against glucose intolerance by increasing beta cell mass.

P2860

Nupr1 deletion protects against glucose intolerance by increasing beta cell mass.

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description

2013 nî lūn-bûn

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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2013年论文

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2013年论文

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name

Nupr1 deletion protects against glucose intolerance by increasing beta cell mass.

@en

Nupr1 deletion protects against glucose intolerance by increasing beta cell mass.

@nl

type

Item

label

Nupr1 deletion protects against glucose intolerance by increasing beta cell mass.

@en

Nupr1 deletion protects against glucose intolerance by increasing beta cell mass.

@nl

prefLabel

Nupr1 deletion protects against glucose intolerance by increasing beta cell mass.

@en

Nupr1 deletion protects against glucose intolerance by increasing beta cell mass.

@nl

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Diabetologia

P1476

Nupr1 deletion protects against glucose intolerance by increasing beta cell mass.

@en

P2093

Ana M Rodriguez de Ledesma

http://www.w3.org/2001/XMLSchema#string

Bo Liu

http://www.w3.org/2001/XMLSchema#string

Cédric Malicet

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Dany S Muller

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James E Bowe

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Juan L Iovanna

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Robert Drynda

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P2860

Cloning and expression of the human p8, a nuclear protein with mitogenic activity

Insulin signalling and the regulation of glucose and lipid metabolism

Regulation of apoptosis by the p8/prothymosin alpha complex

p8 inhibits the growth of human pancreatic cancer cells and its expression is induced through pathways involved in growth inhibition and repressed by factors promoting cell growth

Mice with targeted disruption of p8 gene show increased sensitivity to lipopolysaccharide and DNA microarray analysis of livers reveals an aberrant gene expression response

New perspectives into the molecular pathogenesis and treatment of type 2 diabetes

Cloning and expression of the rat p8 cDNA, a new gene activated in pancreas during the acute phase of pancreatitis, pancreatic development, and regeneration, and which promotes cellular growth

Cell growth-dependent subcellular localization of p8

p8 improves pancreatic response to acute pancreatitis by enhancing the expression of the anti-inflammatory protein pancreatitis-associated protein I

The pro-hypertrophic basic helix-loop-helix protein p8 is degraded by the ubiquitin/proteasome system in a protein kinase B/Akt- and glycogen synthase kinase-3-dependent manner, whereas endothelin induction of p8 mRNA and renal mesangial cell hypert

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s00125-013-3006-x

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2477-2486

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10.1007/S00125-013-3006-X

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23900510

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