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关键词:'07-396'
显示 1-13 共 13 条结果 关于 "07-396" 范围 论文
Lok Hei Chan et al.
Cell reports, 25(3), 690-701 (2018-10-18)
Arginine methylation is a post-translational modification that plays pivotal roles in signal transduction and gene transcription during cell fate determination. We found protein methyltransferase 6 (PRMT6) to be frequently downregulated in hepatocellular carcinoma (HCC) and its expression to negatively correlate
Consalvo Petti et al.
Oncotarget, 6(1), 221-233 (2014-12-05)
Constitutively active receptor tyrosine kinases (RTKs) are known oncogenic drivers and provide valuable therapeutic targets in many cancer types. However, clinical efficacy of RTK inhibitors is limited by intrinsic and acquired resistance. To identify genes conferring resistance to inhibition of
Dectin-1 directs T helper cell differentiation by controlling noncanonical NF-kappaB activation through Raf-1 and Syk.
Sonja I Gringhuis,Jeroen den Dunnen,Manja Litjens,Michiel van der Vlist,Brigitte Wevers et al.
Nature Immunology null
Jennifer A Clark et al.
The Journal of biological chemistry, 279(10), 9233-9247 (2003-12-13)
We have reported previously that protein kinase C (PKC) signaling can mediate a program of cell cycle withdrawal in IEC-18 nontransformed intestinal crypt cells, involving rapid disappearance of cyclin D1, increased expression of Cip/Kip cyclin-dependent kinase inhibitors, and activation of
Jacob R Haling et al.
Cancer cell, 26(3), 402-413 (2014-08-27)
Numerous oncogenic mutations occur within the BRAF kinase domain (BRAF(KD)). Here we show that stable BRAF-MEK1 complexes are enriched in BRAF(WT) and KRAS mutant (MT) cells but not in BRAF(MT) cells. The crystal structure of the BRAF(KD) in a complex
Ivana Yen et al.
Cancer cell, 34(4), 611-625 (2018-10-10)
Targeting KRAS mutant tumors through inhibition of individual downstream pathways has had limited clinical success. Here we report that RAF inhibitors exhibit little efficacy in KRAS mutant tumors. In combination drug screens, MEK and PI3K inhibitors synergized with pan-RAF inhibitors
Kiril Bidzhekov et al.
Journal of cellular and molecular medicine, 11(6), 1395-1407 (2008-01-22)
Mouse embryonic endothelial progenitor cells (eEPCs) acquire a mature phenotype after treatment with cyclic adenosine monophosphate (cAMP), suggesting an involvement of Raf serine/threonine kinases in the differentiation process. To test this idea, we investigated the role of B-Raf and C-Raf
Amardeep S Dhillon et al.
Archives of biochemistry and biophysics, 404(1), 3-9 (2002-07-20)
The Raf-1 kinase is the entry point to the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK-1/2) signaling pathway, which controls fundamental cellular functions including proliferation, differentiation, and survival. As such, Raf-1 is regulated by complex mechanisms that are incompletely understood.
Design and discovery of small molecules targeting raf-1 kinase.
Lowinger, Timothy B, et al.
Current Pharmaceutical Design, 8, 2269-2278 (2002)
L Lin et al.
Cell death and differentiation, 13(11), 1982-1993 (2006-04-01)
Melanoma differentiation-associated gene-5 (mda-5) was the first molecule identified in nature whose encoded protein embodied the unique structural combination of an N-terminal caspase recruitment domain and a C-terminal DExD/H RNA helicase domain. As suggested by its structure, cumulative evidences documented
Yi-Gen Pan et al.
Frontiers in immunology, 8, 1424-1424 (2017-11-23)
The inhibitory effect of immunoreceptor tyrosine-based activation motif (ITAM)-containing adapters DAP12 and FcεRI γ-chain (FcRγ) has been found in many immune functions. Herein, we have further explored the role of these adapters in C-type lectin receptors response. We identified that
Tie-Nian Zhu et al.
The Journal of biological chemistry, 282(20), 14816-14826 (2007-03-29)
The actin-binding protein filamin A (FLNa) is associated with diverse cellular processes such as cell motility and signaling through its scaffolding properties. Here we examine the effect of FLNa on the regulation of signaling pathways that control the expression of
Avinashnarayan Venkatanarayan et al.
Cell reports, 38(6), 110351-110351 (2022-02-10)
KRAS, which is mutated in ∼30% of all cancers, activates the RAF-MEK-ERK signaling cascade. CRAF is required for growth of KRAS mutant lung tumors, but the requirement for CRAF kinase activity is unknown. Here, we show that subsets of KRAS
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