Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
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
This study demonstrated that Oligodendrocyte RasG12V expressed in its endogenous locus disrupts myelin structure through increased MAPK (show MAPK1 Antibodies), nitric oxide, and notch (show NOTCH1 Antibodies) signaling.
Data indicate dynamic of H-Ras functional cycle as controlled by son of sevenless homolog 1 (show SOS1 Antibodies) (Sos).
Our data support the idea that a variable range of dysregulated HRAS-dependent signalling dynamics, rather than static activation of HRAS-dependent signal flow, may underlie the phenotypic variability in CS.
AF6 (show MLLT4 Antibodies) employs a non-canonical, evolutionarily conserved alpha-helix to bind RAS, unique to AF6 (show MLLT4 Antibodies) and the classical RASSF effectors.
Case Report: somatic HRAS mutation in pigmented trichoblastoma developed in a sebaceous nevus.
our identification of the novel interaction between Aurora A (show AURKA Antibodies) and H-Ras as a mechanism by which Aurora A (show AURKA Antibodies) can activate Ras-MAPK (show MAPK1 Antibodies) signaling opens the way for studies into perturbation of the Aurora A (show AURKA Antibodies)/H-Ras interaction and the effect on Ras-MAPK (show MAPK1 Antibodies) signaling.
Peroxiredoxin I (Prx (show PRDX6 Antibodies) I) increased in tumors of hepatocellular carcinoma (HCC (show FAM126A Antibodies)) patients that aligned with overexpression of oncogenic H-ras.
Familial alcohol dependence was associated with hypomethylation of CpG sites in the HRAS promoter region.
Suppression of MEK/ERK pathway in senescent cells provides a new strategy for elimination of Ras-expressing cells.
ESR1 inhibits senescence-like phenotype and facilitates transformation induced by oncogenic ras in human mammary epithelial cells
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 belongs to the Ras oncogene family, whose members are related to the transforming genes of mammalian sarcoma retroviruses. The products encoded by these genes function in signal transduction pathways. These proteins can bind GTP and GDP, and they have intrinsic GTPase activity. This protein undergoes a continuous cycle of de- and re-palmitoylation, which regulates its rapid exchange between the plasma membrane and the Golgi apparatus. Mutations in this gene cause Costello syndrome, a disease characterized by increased growth at the prenatal stage, growth deficiency at the postnatal stage, predisposition to tumor formation, mental retardation, skin and musculoskeletal abnormalities, distinctive facial appearance and cardiovascular abnormalities. Defects in this gene are implicated in a variety of cancers, including bladder cancer, follicular thyroid cancer, and oral squamous cell carcinoma. Multiple transcript variants, which encode different isoforms, have been identified for this gene.
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
, H-ras 1 protein
, c-Ha-ras p21 protein
, c-Ha-ras transgene
, transforming protein P21