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September 1, 2000DiabetesOpen Access

The c-Jun amino-terminal kinase pathway is preferentially activated by interleukin-1 and controls apoptosis in differentiating pancreatic beta-cells.

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Authors

AAA AmmendrupAMAnne MaillardKNKristina Tomra Nielsen

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Ammendrup et al. (2000) studied this question.

synapsesocial.com/papers/6a956f6b6a42edee3f2caf43https://doi.org/10.2337/diabetes.49.9.1468
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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  2. 2Role for p38 Mitogen-activated Protein Kinase in Platelet Aggregation Caused by Collagen or a Thromboxane Analogue1996 · 294 citations
  3. 3β-Cell-specific inactivation of the mouse<i>Ipf1/Pdx1</i> gene results in loss of the β-cell phenotype and maturity onset diabetes1998 · 921 citations
  4. 4jun N-terminal Kinase Mediates Activation of Skeletal Muscle Glycogen Synthase by Insulin in Vivo1996 · 112 citations
  5. 5Apoptosis contributes to the involution of beta cell mass in the post partum rat pancreas.1995 · 210 citations