The c-Jun NH2-terminal kinase (JNK) is activated during obesity. One consequence of obesity is that JNK phosphorylates the adapter protein insulin receptor substrate 1 (IRS-1) on Ser 307 and inhibits signaling by the insulin receptor. JNK can therefore cause peripheral insulin resistance during obesity and may contribute to the development of type 2 diabetes. Here we report that the JNK-interacting protein 1 (JIP1) scaffold protein, which binds components of the JNK signaling module, is essential for JNK activation in the adipose tissue of obese mice. These data identify JIP1 as a novel molecular target for therapeutic intervention in the development of obesity
Activation of stress-kinase signaling has recently been recognized as an important pathophysiologica...
Scaffold proteins have been established as important mediators of signal transduction specificity. T...
SummaryActivation of c-Jun N-terminal kinase 1 (JNK1)- and inhibitor of nuclear factor kappa-B kinas...
The c-Jun NH(2)-terminal kinase (JNK) interacting protein 1 (JIP1) has been proposed to act as a sca...
Obesity is a major risk factor for the development of metabolic syndrome and type 2 diabetes. How ob...
Obesity and associated metabolic disturbances, such as increased circulating fatty acids cause prolo...
Obesity and associated metabolic disturbances, such as increased circulating fatty acids cause prolo...
The cJun NH(2)-terminal kinase isoform JNK1 is implicated in the mechanism of obesity-induced insuli...
SummaryObesity-induced insulin resistance is a major factor in the etiology of type 2 diabetes, and ...
A high-fat diet causes activation of the regulatory protein c-Jun NH2-terminal kinase 1 (JNK1) and t...
Obesity caused by feeding of a high-fat diet (HFD) is associated with an increased activation of c-J...
OBJECTIVE - Obesity is associated with increased activation of the c-Jun NH2-terminal kinase (JNK) i...
OBJECTIVE Obesity is associated with increased activation of the c-Jun NH2-terminal kinase (JNK) in ...
OBJECTIVE Obesity is associated with increased activation of the c-Jun NH2-terminal kinase (JNK) in ...
Proper functioning of endocrine cells is crucial for organismal homeostasis. The underlying mechanis...
Activation of stress-kinase signaling has recently been recognized as an important pathophysiologica...
Scaffold proteins have been established as important mediators of signal transduction specificity. T...
SummaryActivation of c-Jun N-terminal kinase 1 (JNK1)- and inhibitor of nuclear factor kappa-B kinas...
The c-Jun NH(2)-terminal kinase (JNK) interacting protein 1 (JIP1) has been proposed to act as a sca...
Obesity is a major risk factor for the development of metabolic syndrome and type 2 diabetes. How ob...
Obesity and associated metabolic disturbances, such as increased circulating fatty acids cause prolo...
Obesity and associated metabolic disturbances, such as increased circulating fatty acids cause prolo...
The cJun NH(2)-terminal kinase isoform JNK1 is implicated in the mechanism of obesity-induced insuli...
SummaryObesity-induced insulin resistance is a major factor in the etiology of type 2 diabetes, and ...
A high-fat diet causes activation of the regulatory protein c-Jun NH2-terminal kinase 1 (JNK1) and t...
Obesity caused by feeding of a high-fat diet (HFD) is associated with an increased activation of c-J...
OBJECTIVE - Obesity is associated with increased activation of the c-Jun NH2-terminal kinase (JNK) i...
OBJECTIVE Obesity is associated with increased activation of the c-Jun NH2-terminal kinase (JNK) in ...
OBJECTIVE Obesity is associated with increased activation of the c-Jun NH2-terminal kinase (JNK) in ...
Proper functioning of endocrine cells is crucial for organismal homeostasis. The underlying mechanis...
Activation of stress-kinase signaling has recently been recognized as an important pathophysiologica...
Scaffold proteins have been established as important mediators of signal transduction specificity. T...
SummaryActivation of c-Jun N-terminal kinase 1 (JNK1)- and inhibitor of nuclear factor kappa-B kinas...