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Human RAF1 Protein expressed in Wheat germ - ABIN1317314
Rodríguez-Muñoz, de la Torre-Madrid, Sánchez-Blázquez, Garzón: NO-released zinc supports the simultaneous binding of Raf-1 and PKC? cysteine-rich domains to HINT1 protein at the mu-opioid receptor. dans Antioxidants & redox signaling 2011
The functional assessment supported the pathogenicity of the RAF1 and RIT1 VUSs, while the significance of two variants of unknown significance in A2ML1 remained unclear.
Our report presents the second familial case of Noonan syndrome due to a germline p.S427G substitution in RAF] with no occurrence of a malignant tumor. It may suggest that carrying a germline mutation in the RAF1 oncogene is not associated with an increased risk of tumor development. Since RAF1 mutations have been observed as a somatic event in many types of cancer.
Data indicate that Raf-1 proto-oncogene, serine-threonine kinase (RAF1) is a negative regulator of hepatocarcinogenesis.
we report a patient with an inherited RAF1-associated Noonan syndrome, presenting with an antenatally diagnosed abnormality of skull shape, bilateral subdural haematomas, of unknown cause, delayed myelination and polymicrogyria.
Raf1 may serve as a novel prognostic factor and potential target for improving the longterm outcome of nonsmall cell lung cancer (NSCLC).
Results provide evidence that RAF1 binding to SPRY4 is regulated by miR-1908 in glioma tumors.
High RAF1 expression is associated with malignant melanoma.
two premature neonates with progressive biventricular hypertrophy found to have RAF1 variants in the CR2 domain, are reported.
Data indicate connector enhancer of kinase suppressor of Ras 1 protein (CNK1) as a molecular platform that controls c-raf protein (RAF) and c-akt protein (AKT) signalling and determines cell fate decisions in a cell type- and cell stage-dependent manner.
CRAF is a bona fide alternative oncogene for BRAF/NRAS/GNAQ/GNA11 wild type melanomas
Authors evaluated the expression of known targets of miR-125a and found that sirtuin-7, matrix metalloproteinase-11, and c-Raf were up-regulated in tumor tissue by 2.2-, 3-, and 1.7-fold, respectively. Overall, these data support a tumor suppressor role for miR-125a.
Overexpression of ciRS-7 in HCT116 and HT29 cells led to the blocking of miR-7 and resulted in a more aggressive oncogenic phenotype, and ciRS-7 overexpression permitted the inhibition of miR-7 and subsequent activation of EGFR and RAF1 oncogenes
miR-497 could serve as a tumor suppressor and a potential early diagnostic marker of gastric cancer by targeting Raf-1 proto-oncogene.
RAF1 may have a role in survival in hepatocellular carcinoma, and indicate whether sorafenib should be used as a postoperative adjuvant
Mutational activation of Kit-, Ras/Raf/Erk- and Akt- pathways indicate the biological importance of these pathways and their components as potential targets for therapy.
Results indicate that des-gamma-carboxy prothrombin (DCP) antagonizes the inhibitory effects of Sorafenib on hepatocellular carcinoma (HCC) through activation of the Raf/MEK/ERK and PI3K/Akt/mTOR signaling pathways.
DiRas3 binds to KSR1 independently of its interaction with activated Ras and RAF.
RhoA/ROCK and Raf-1/CK2 pathway are responsible for TNF-alpha-mediated endothelial cytotoxicity via regulation of the vimentin cytoskeleton.
Although Raf-1 gene is not mutated, an abnormality of Raf-1 kinase feedback regulation enhances its antiapoptotic function, and Raf-1 can still be a pharmaceutical target to increase chemotherapy or radiotherapy sensitivity in these cancer cells.
RAF1 plays a critical role in maintaining the transformed phenotype of CRC cells, including those with mutated KRAS.
cdk10 has roles in vertebrate development and a critical function in neurogenesis by modulation of raf1a expression
Our results indicate that Rb-Raf-1 interaction plays an important role in spontaneous hair cell regeneration in zebrafish
Zebrafish embryos with morpholino knockdown of raf1 demonstrated the need for raf1 for the development of normal myocardial structure and function.
analysis of the roles of Raf- and PI3K-signalling pathways in melanoma
data suggest that G alpha(i3), Shc, Grb2, Ras, and Raf-1 link Src to activation of MAPK and to the AT(2)-dependent increase in eNOS expression in PAECs
that ablation of c-RAF expression in advanced tumors driven by Kras(G12V)/Trp53 mutations leads to significant tumor regression with no detectable appearance of resistance mechanisms
Results indicate specific and compensatory functions for proto-oncogene B-Raf (BRAF) and proto-oncogene c-RAF (CRAF) and highlight an addiction to RAF signalling in NRAS-driven melanoma.
Our findings indicated that miR-195 inhibited WT and L613V RAF-1 induced hyperactive osteoblast differentiation in MC3T3-E1 cells by targeting RAF-1
Results indicate that proto-oncogene c-RAF (CRAF) function affects postmitotic neural cell differentiation and points to a critical role of CRAF-dependent growth factor signaling pathway in the postmitotic development of adult-born neurons.
our studies demonstrate that PDE8A inhibition by enzymatic inhibitors or PDE8A-Raf-1 kinase complex disruptors decreases Teff cell adhesion and migration under flow, and represents a novel approach to target T cells in inflammation
BRAF and ROKalpha form independent RAF1 complexes in embryonic fibroblasts (MEFs) treated with epidermal growth factor (EGF).
Mechanistically, BRAF and RAF1 operate independently to balance MAPK signaling: BRAF promotes ERK activation, while RAF1 dims stress kinase activation.
Neuroprotective (arylthio)cyclopentenone prostaglandins directly bind to c-Raf protein and protect cells from down-regulation of the c-Raf protein itself, resulting in protection against oxidative stress.
A- and B-Raf ablation in chondrocytes does not alter skeletal development, whereas ablation of C-Raf decreases hypertrophic chondrocyte apoptosis and impairs vascularization of the growth plate. However, ablation of C-Raf does not impair phosphate-induced ERK1/2 phosphorylation in vitro, but leads to rickets by decreasing VEGF protein stability.
We confirmed that Raf1(L613V) knock-in confers a NS-like phenotype, including cardiac hypertrophy. Active RSK3 was increased in Raf1(L613V) mice. Constitutive RSK3 gene deletion prevented the Raf1(L613V)-dependent concentric growth in width of the cardiac myocyte and attenuated cardiac hypertrophy in female mice.
C-Raf involves in osteoblast survival in response to mechanical stress.
Dual inhibition of c-Raf and soluble epoxide hydrolase by t-CUPM prevents mutant KrasG12D-initiated murine pancreatic carcinoma growth.
Simultaneous inhibition of sEH and c-RAF prevents chronic pancreatitis and murine pancreatic intraepithelial neoplasia in LSL-KrasG(1)(2)D/Pdx-1-Cre mice.
under normal physiological conditions, PTEN suppresses AKT activity to maintain activation of the RAF1/ERK signaling pathway, which in turn maintains normal function of the initial segment and therefore, normal sperm maturation.
these data indicate that B-RAF is an important factor in oncogenic C-RAF-mediated tumorigenesis.
PHLPP is a negative regulator of RAF1, which reduces colorectal cancer cell motility and prevents tumor progression in mice.
Raf-MAPK-dependent psoriatic-like epidermal hyperplasia requires Stat3 signaling in keratinocytes
Computational modeling revealed that complexes containing H-ras conformers and galectin-1 affect both the number and lifetime of nanoclusters and thus determine the specific Raf effector recruitment.
This EPOR/CR3 system may serve as a useful model to evaluate the unknown Raf kinase pathway and the effects of signal transduction inhibitors for Raf as a target
Both c-Raf and B-Raf are required for Ras-induced MEK1 and p42 MAP kinase activation.
This gene is the cellular homolog of viral raf gene (v-raf). The encoded protein is a MAP kinase kinase kinase (MAP3K), which functions downstream of the Ras family of membrane associated GTPases to which it binds directly. Once activated, the cellular RAF1 protein can phosphorylate to activate the dual specificity protein kinases MEK1 and MEK2, which in turn phosphorylate to activate the serine/threonine specific protein kinases, ERK1 and ERK2. Activated ERKs are pleiotropic effectors of cell physiology and play an important role in the control of gene expression involved in the cell division cycle, apoptosis, cell differentiation and cell migration. Mutations in this gene are associated with Noonan syndrome 5 and LEOPARD syndrome 2.
, RAF proto-oncogene serine/threonine-protein kinase
, proto-oncogene c-RAF
, raf proto-oncogene serine/threonine protein kinase
, murine leukemia viral (v-raf-1) oncogene homolog 1 (3611-MSV)
, v-raf-1 murine leukemia viral oncogene homolog 1
, murine leukemia viral oncogene homolog
, serine/threonine protein kinase RAF1
, MIL proto-oncogene serine/threonine-protein kinase
, c-mil protein
, murine leukemia viral (v-raf-1) oncogene homolog 1
, RAF proto-oncogene serine/threonine-protein kinase-like
, Craf1 transforming
, murine sarcoma 3611 oncogene 1
, sarcoma 3611 oncogene
, v-raf-1 leukemia viral oncogene 1
, Proto-oncogene c-RAF