EGFRvIII is constitutively active thus it does not require the ligand EGF for activation. Our work demonstrates that it also highly activates the PI3K pathway, where the wildtype EGFR is better known for its activation of ERK. Our efforts on signaling pathways have discovered that glioblastoma tumors preferentially utilize the JNK pathway, unlike many other tumors that use the ERK pathway. More specifically, only one of the 12 known JNK isoforms is highly expressed, JNK2a2. Co-incidentally, we have uncovered that this isoform is constitutively active and that it has a specific activation domain. JNK2a2 also upregulates TGF-a, a ligand for the EGF receptor that is frequently overexpressed in glioblastomas. Our additional basic science studies to understand EGFRvIII signaling led us to discover the Gab1 docking protein. Originally discovered as a docking protein substrate for both EGF and Insulin receptors, it is now known as a substrate for multiple receptors vital for growth factor and cytokine ...

In the present study we identified and characterized the docking domains of a novel JNK-binding protein, WDR62. Mutations in WDR62 are found to cause deleterious phenotypes such as microcephaly and pachygyria [10,22,23].. JNK proteins play a major role in multiple stress responses and regulate diverse cellular functions. JNKs are part of the MAPK cascade mediated through association with MAP2Ks (MKK4/7) and MAP3Ks. JNK also associates with MAPK phosphatases as well as with various cellular substrates [24-26]. In addition, JNK proteins associate with scaffold proteins that also mediate binding to additional pathway components. Scaffolds facilitate and direct signalling to various cellular compartments [3]. WDR62 is a novel scaffold protein identified on the basis of its ability to associate with JNK in a yeast two-hybrid screen [9,27]. WDR62 was found to be recruited to cellular granules that are formed following cellular exposure to arsenite. The recruitment of WDR62 to stress granules and JNK ...

LA JOLLA, Calif., - Put simply, a tumor is the result of out-of-control cell growth. To assure that the cell cycle - the cells process of duplicating itself to make more cells - goes smoothly, a large network of proteins tells other proteins what to do and when to do it. When any of these layers of protein regulation fail, cell growth can get out of hand. A new study led by Zeev Ronai, Ph.D., associate director of Sanford-Burnhams National Cancer Institute-designated Cancer Center, reveals a new player in cell cycle control. These findings, which appeared online in Nature Cell Biology on June 27, showed that JNK, a protein already well known for other duties, also regulates the cell cycle.. This was totally unexpected of JNK, explained Gustavo Gutierrez, Ph.D., postdoctoral researcher in Dr. Ronais laboratory and first author of the study. We already knew that JNK helps cells respond to stress, such as damage caused by ultraviolet radiation. We thought we already knew how the major ...

The c-Jun N-terminal protein kinase signaling pathway mediates Bax activation and subsequent neuronal apoptosis in the course interaction with Bim after transitory centred cerebral ischemia. High internal tension of the bladder has a occasion likelihood to d‚nouement develop in bladderВ-ureter reflux and harm the kidney in a retrograde frame, which is the dean origin of cessation for the benefit of the new produce of SCI [9, 10]. Unfortunately, Pneumovax 23 does not protect against nonbacteremic disease (ie, pneumonia without bloodstream infection) (French et al 2000; Whitney et al 2003) buy 5 mg zyrtec with visa allergy medicine 4h2. When a neonate who has previously been diagnosed with an innate mistaken of metabolism is hospitalized, the sister must decide the prescribed fast and medications so these may be continued while in the sickbay setting. On place against, another over inaugurate a significant reduction in the troop of rapid ripples recorded with pier clinical electrodes ...

2671 Chronic alcohol drinking can damage many organs including liver, pancreas, and brain. In addition, numerous studies suggest that ethanol can damage various cells in culture. However, the mechanism of cell or organ damage is still poorly understood with respect to early signaling cascades including mitogen activated protein (MAP) kinases. Therefore, we hypothesized that changes in the early signaling cascades are critically important in ethanol-mediated cell death. In this study, we investigate the role of the MAP kinases during ethanol-induced damage to SK-N-SH neuroblastoma cells. Ethanol caused time- and dose-dependent cell death in SK-N-SH cells. Ethanol increased c-Jun N-terminal protein kinase (JNK) activity in a time- and concentration dependent manner. Within 15 min after ethanol exposure, JNK activity increased and the elevated JNK activity persisted until 16 h after exposure to ethanol. In contrast, p38 kinase activity was transiently increased between 15 min and 4 h after ethanol ...

Cytokines and stress-inducing stimuli signal through c-Jun N-terminal kinase (JNK) using a diverse and only partially defined set of downstream effectors. In ...

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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-Jun N-terminal protein kinase (JNK). Moreover, flow cytometry indicated that ectopically overexpressed c-Jun in conjunction with tylophorine significantly increased the number of carcinoma cells that were arrested at the G1 phase. The tylophorine-mediated downregulation of cyclin A2 protein levels is known to be involved in the primary G1 arrest. Chromatin immunoprecipitation and reporter assays revealed that tylophorine enhanced the c-Jun downregulation of the cyclin A2 promoter activity upon increased binding of c-Jun to the deregulation AP1 site and decreased binding to the upregulation activating transcription factor (ATF) site in the cyclin A2 ...

Melanoma differentiation associated gene-7/interleukin-24 (mda-7/IL-24) is a novel cytokine displaying selective apoptosis-inducing activity in transformed cells without harming normal cells. The present studies focused on clarifying the mechanism(s) by which glutathione S-transferase (GST)-MDA-7 altered cell survival of human renal carcinoma cells in vitro. GST-MDA-7 caused plasma membrane clustering of CD95 and the association of CD95 with procaspase-8. GST-MDA-7 lethality was suppressed by inhibition of caspase-8 or by overexpression of short-form cellular FLICE inhibitory protein, but only weakly by inhibition of cathepsin proteases. GST-MDA-7-induced CD95 clustering (and apoptosis) was blocked by knockdown of acidic sphingomyelinase or, to a greater extent, ceramide synthase-6 expression. GST-MDA-7 killing was, in parallel, dependent on inactivation of extracellular signal-regulated kinase 1/2 and on CD95-induced p38 mitogen-activated protein kinase and c-jun NH2-terminal kinase-1/2 ...

Background/Aims: aberrant c-Jun N-terminal kinase (JNK) activation has been linked to hepatocellular carcinoma (HCC) in mouse models. It remains unclear whether JNK activation plays an important role in human HCC and, if so, how JNK signaling contributes to the initiation or progression of HCC. Methods: the JNK activation, global gene expression, and the status of histone H3 methylations were mea