Results 21 to 30 of about 521,522 (308)

Thrombin Protease-activated Receptor-1 Signals through Gq- and G13-initiated MAPK Cascades Regulating c-Jun Expression to Induce Cell Transformation [PDF]

open access: yes, 2003
Although the ability of G protein-coupled receptors to stimulate normal and aberrant cell growth has been intensely investigated, the precise nature of the molecular mechanisms underlying their transforming potential are still not fully understood.
Gutkind, J. Silvio   +4 more
core   +1 more source

Investigation of c-Jun N-terminal Kinase 2 Regulation [PDF]

open access: yes, 2017
JNK2). This protein is unique in that it can autophosphorylate, or phosphorylate itself. It was found that these proteins tend to form aggregates of four, or tetramers, when inactive and remain as single units, or monomers, when active.
Go, Jaeeun
core   +1 more source

Protein Kinase R Modulates c-Fos and c-Jun Signaling to Promote Proliferation of Hepatocellular Carcinoma with Hepatitis C Virus Infection [PDF]

open access: yes, 2013
Double-stranded RNA-activated protein kinase R (PKR) is known to be upregulated by hepatitis C virus (HCV) and overexpressed in hepatocellular carcinoma (HCC). However, the precise roles of PKR in HCC with HCV infection remain unclear.
Abe, Masanori   +8 more
core   +8 more sources

c-Jun-mediated anticancer mechanisms of tylophorine [PDF]

open access: yesCarcinogenesis, 2013
Tylophorine, a phenanthroindolizidine alkaloid, is the major medicinal constituent of herb Tylophora indica. Tylophorine treatment increased the accumulation of c-Jun protein, a component of activator protein 1 (AP1), in carcinoma cells. An in vitro kinase assay revealed that the resultant c-Jun phosphorylation was primarily mediated via activated c ...
Cheng-Wei, Yang   +6 more
openaire   +2 more sources

Regulation of anti-inflammatory gene expression in vascular endothelial cells by EPAC1 [PDF]

open access: yes, 2015
Suppressor of cytokine signalling 3 (SOCS3) is a potent inhibitor of pro-inflammatory pathways involved in atherogenesis and the development of neo-intimal hyperplasia (NIH), which contributes to the in-stent re-stenosis responsible for the failure of ...
Palmer, Timothy P., Yarwood, Stephen J.
core   +1 more source

Hepatic c-Jun regulates glucose metabolism via FGF21 and modulates body temperature through the neural signals

open access: yesMolecular Metabolism, 2019
Objective: c-Jun, a prominent member of the activator protein 1 (AP-1) family, is involved in various physiology processes such as cell death and survival. However, a role of hepatic c-Jun in the whole-body metabolism is poorly understood.
Fei Xiao   +17 more
doaj   +1 more source

c-Jun N-Terminal Kinase in Inflammation and Rheumatic Diseases. [PDF]

open access: yes, 2012
The c-Jun N-terminal kinases (JNKs) are members of the mitogen-activated protein kinase (MAPK) family and are activated by environmental stress. JNK is also activated by proinflammatory cytokines, such as TNF and IL-1, and Toll-like receptor ligands ...
Firestein, Gary S, Guma, Monica
core   +1 more source

JunD, not c-Jun, is the AP-1 transcription factor required for Ras-induced lung cancer

open access: yesJCI Insight, 2021
The AP-1 transcription factor c-Jun is required for Ras-driven tumorigenesis in many tissues and is considered as a classical proto-oncogene. To determine the requirement for c-Jun in a mouse model of K-RasG12D–induced lung adenocarcinoma, we inducibly ...
E. Josue Ruiz   +12 more
doaj   +1 more source

C-junInhibits Mammary Apoptosis In Vivo [PDF]

open access: yesMolecular Biology of the Cell, 2010
c-jun, which is overexpressed in a number of human cancers encodes a critical component of the AP-1 complex. c-jun has been shown to either induce or inhibit cellular apoptosis. Germ line deletion of both c-jun alleles is embryonically lethal. To determine the role of the endogenous c-jun gene in apoptosis, we performed mammary epithelial cell–targeted
Katiyar, Sanjay   +6 more
openaire   +2 more sources

Induction of c-Jun immunoreactivity in spinal cord and brainstem neurons in a transgenic mouse model for amyotrophic lateral sclerosis [PDF]

open access: yes, 1996
Transgenic mice carrying amyotrophic lateral sclerosis (ALS)-linked superoxide dismutase 1 (SOD1) mutations develop a motoneuron disease resembling human ALS. c-Jun is a transcription factor frequently induced in injured neurons.
Davis, M. (Maria)   +6 more
core   +1 more source

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