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anti-Human HRAS Antibodies:
anti-Rat (Rattus) HRAS Antibodies:
anti-Mouse (Murine) HRAS Antibodies:
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Human Polyclonal HRAS Primary Antibody for IF, IHC (p) - ABIN392183
Ma, Liu, Wu, Terada: p66(Shc) restrains Ras hyperactivation and suppresses metastatic behavior. in Oncogene 2010
Show all 2 Pubmed References
Human Polyclonal HRAS Primary Antibody for ELISA, WB - ABIN561363
Ambrosini, Khanin, Carvajal, Schwartz: Overexpression of DDX43 mediates MEK inhibitor resistance through RAS Upregulation in uveal melanoma cells. in Molecular cancer therapeutics 2014
Authors analyzed 421 samples from CLM patients for their all-RAS mutation status to compare the overall survival rate (OS), recurrence-free survival rate (RFS), and the pattern of recurrence between the patients with and without RAS mutations.
A quantitative, mutation-enrichment next-generation sequencing test for detecting KRAS(G12/G13) mutations in urine cfDNA had good concordance with testing of archival tumor tissue. Changes in mutated urine cfDNA were associated with time to treatment failure.
Findings indicate neurofibromin 1 (NF1 (show NF1 Antibodies)) as the most frequently occurring driver mutation in mucosal melanoma, and RAS alterations, consisting of NRAS (show NRAS Antibodies) and KRAS mutations, were the second most frequent mutation type.
Case Report: somatic HRAS mutation in pigmented trichoblastoma developed in a sebaceous nevus.
AFR3 cells harbored the secondary EGFR mutation T790M. Our findings constitute the first report showing acquired wild-type KRAS overexpression and attenuation of afatinib resistance following a drug holiday. The heterogeneous mechanisms of afatinib resistance should facilitate the development of more effective therapeutic strategies for non-small cell lung cancer patients
that conventional cytology from Endoscopic ultrasound-guided fine-needle aspiration samples is highly specific for the diagnosis of KRAS mutation in pancreatic cancer
KRAS Polymorphism is associated with recurrence in non-small cell lung cancer.
The study results improve our understanding of the ATMIN-KRas axis leading to HNSCC migration or invasion and metastasis and facilitates the identification of possible therapy targets of downstream genes for designing effective therapeutic strategies in personalized medicine
miR-450b-5p induced by oncogenic KRAS is required for colorectal cancer progression
The critical roles of miR-30a and ME1 in the development of KRAS-mutant colorectal cancer indicate therapy potentials for this subtype of cancer.
Kita driven expression of oncogenic HRAS leads to early onset and highly penetrant melanoma in zebrafish
Data demonstrate that H-Ras activation is important in the activation of the specific signaling events leading to the accelerated retinal capillary cell apoptosis in hyperglycemic conditions.
Activation of H-Ras and its downstream signaling pathway in the retina and its vasculature could be under the control of superoxide, and H-Ras activation in diabetes can be prevented by inhibiting superoxide accumulation.
Thrombospondin 1 (show THBS1 Antibodies), fibronectin (show FN1 Antibodies), and vitronectin (show VTN Antibodies) are differentially dependent upon RAS, ERK1/2, and p38 (show MAPK14 Antibodies) for induction of vascular smooth muscle cell chemotaxis.
Loss of wild-type Hras promotes the earliest stages of pancreatic tumorigenesis, and moreover results in more rapid progression of the disease. As such, mechanisms leading to activation of wild-type Ras proteins, including but not limited to redox-dependent reactions, may influence the development of pancreatic cancer.
High HRAS expression is associated with hepatocarcinogenesis.
p21 (show D4S234E Antibodies)-associated inhibition of early-stage malignant progression and the intense expression in papilloma outgrowths, identifies a novel, significant antagonism between p21 (show D4S234E Antibodies) and ras(Ha)/ROCK2 (show ROCK2 Antibodies)/NF-kappaB (show NFKB1 Antibodies) signalling in skin carcinogenesis.these data show that ROCK2 (show ROCK2 Antibodies) activation induces malignancy in ras(Ha)-initiated/promoted papillomas in the context of p53 (show TP53 Antibodies) loss and novel NF-kappaB (show NFKB1 Antibodies) expression
this study shows that retinoic acid stabilizes HRas protein during neurogenesis.
we provide genetic evidence that the wild-type H-Ras and K-Ras proteins are bioequivalent in spite of their different structural and biological properties
loss of one allele of Hras increased the sensitivity of mice to this carcinogen, and this effect was further exacerbated by the loss of the second Hras allele. However, loss of one or both alleles of Nras (show NRAS Antibodies) failed to alter tumor burden, either in the absence or presence of Hras, after exposure to urethane.
H-ras isoform mediates protection against pressure overload-induced cardiac dysfunction in part through activation of AKT (show AKT1 Antibodies)/PI3K signaling pathway.
The long intergenic non-coding RNA CCR492 functions as a let-7 competitive endogenous RNA to de-repress c-Myc (show MYC Antibodies) expression and to promote cell transformation assisted by the constitutively active H-Ras.
these contrasting signatures precisely match those proposed to confer bias toward Hras(CAA61CTA) versus Braf (show BRAF Antibodies)(GTG636GAG) mutations in the original tumor sets. Our findings highlight a novel mechanism whereby exposure history acts through strand-biased mutagenesis to specify activation of preferred oncogenes
The abnormal expression of epidermal cytokeratins suggests that Ha-Ras and Bcl-2 (show BCL2 Antibodies) suppress the terminal differentiation and sustain the stem cell-like features in epidermal keratinocytes
This gene, a Kirsten ras oncogene homolog from the mammalian ras gene family, encodes a protein that is a member of the small GTPase superfamily. A single amino acid substitution is responsible for an activating mutation. The transforming protein that results is implicated in various malignancies, including lung adenocarcinoma, mucinous adenoma, ductal carcinoma of the pancreas and colorectal carcinoma. Alternative splicing leads to variants encoding two isoforms that differ in the C-terminal region.
GTP- and GDP-binding peptide B
, GTPase HRas
, Ha-Ras1 proto-oncoprotein
, Ras family small GTP binding protein H-Ras
, c-has/bas p21 protein
, c-ras-Ki-2 activated oncogene
, p19 H-RasIDX protein
, transformation gene: oncogene HAMSV
, transforming protein p21
, v-Ha-ras Harvey rat sarcoma viral oncogene homolog
, Transforming protein p21
, neuroblastoma ras oncogene
, v-Ha-ras Harvey rat sarcoma viral oncogene-like protein
, Harvey ras1 protein
, Harvey rat sarcoma viral (v-Ha-ras) oncogene homolog
, ras p21
, small G-protein H-Ras
, GTPase HRas (Transforming protein p21) (H-Ras-1) (c-H-ras)
, Harvey ras 1
, GTPase KRas
, K-Ras 2
, K-ras p21 protein
, PR310 c-K-ras oncogene
, c-Kirsten-ras protein
, cellular c-Ki-ras2 proto-oncogene
, oncogene KRAS2
, v-Ki-ras2 Kirsten rat sarcoma 2 viral oncogene homolog
, v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog
, H-ras 1 protein
, c-Ha-ras p21 protein
, c-Ha-ras transgene
, transforming protein P21