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Key Documents

SAB1405964

Sigma-Aldrich

Anti-HRAS antibody produced in mouse

purified immunoglobulin, buffered aqueous solution

Sinónimos:

C-BAS/HAS, C-H-RAS, C-HA-RAS1, CTLO, H-RASIDX, HAMSV, HRAS1, K-RAS, N-RAS

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~20.79 kDa

species reactivity

human

technique(s)

proximity ligation assay: suitable
western blot: 1 μg/mL

NCBI accession no.

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... HRAS(3265)

General description

Harvey rat sarcoma viral oncogene homolog (HRAS) is a member of the Ras oncogene family. The HRAS gene is mapped to human chromosome 11p15.5 and is expressed in different isoforms. HRAS comprises a conserved G domain and a hypervariable region. The G domain, in turn, contains switch I and II domains. It also harbors the secondary signal domain and the CAAX motif. The HRAS protein is localized to the Golgi membrane.

Immunogen

HRAS (NP_005334, 1 a.a. ~ 189 a.a) full-length human protein.

Sequence
MTEYKLVVVGAGGVGKSALTIQLIQNHFVDEYDPTIEDSYRKQVVIDGETCLLDILDTAGQEEYSAMRDQYMRTGEGFLCVFAINNTKSFEDIHQYREQIKRVKDSDDVPMVLVGNKCDLAARTVESRQAQDLARSYGIPYIETSAKTRQGVEDAFYTLVREIRQHKLRKLNPPDESGPGCMSCKCVLS

Application

Anti-HRAS antibody produced in mouse has been used in western blotting.

Biochem/physiol Actions

Harvey rat sarcoma viral oncogene homolog (HRAS) exists as guanosine triphosphate (GTP)-bound form when associated with non-ordered lipid domains. However, with the lipid rafts of the plasma membrane, HRAS is present in a guanosine diphosphate (GDP)-bound state. It regulates the signaling events in a wide variety of cellular processes. Germline mutations in the HRAS gene results in Costello syndrome, a disease with cardiovascular abnormalities, growth deficiency, and musculoskeletal abnormalities. The HRAS gene defects are also implicated in the pathophysiology of many tumors including epithelial-myoepithelial carcinoma (EMC), thyroid, oral squamous cell carcinoma, and bladder cancer.

Physical form

Solution in phosphate buffered saline, pH 7.4

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class

10 - Combustible liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Lihua Shu et al.
Molecular cancer therapeutics, 19(4), 999-1007 (2020-04-04)
H-Ras is a unique isoform of the Ras GTPase family, one of the most prominently mutated oncogene families across the cancer landscape. Relative to other isoforms, though, mutations of H-Ras account for the smallest proportion of mutant Ras cancers. Yet
Christian P Kratz et al.
Human molecular genetics, 16(4), 374-379 (2006-12-14)
Costello syndrome (CS; MIM 218040) is characterized by short stature, facial dysmorphism, cardiac defects and predisposition to embryonal rhabdomyosarcoma (CS/ERMS) and other neoplasias. CS is caused by germline mutations in the HRAS gene on chromosome 11p15.5, a region showing allelic
Anne-Mette Hartung et al.
PLoS genetics, 12(5), e1006039-e1006039 (2016-05-20)
Costello syndrome (CS) may be caused by activating mutations in codon 12/13 of the HRAS proto-oncogene. HRAS p.Gly12Val mutations have the highest transforming activity, are very frequent in cancers, but very rare in CS, where they are reported to cause
G Aaron Hobbs et al.
Journal of cell science, 129(7), 1287-1292 (2016-03-18)
RAS proteins (KRAS4A, KRAS4B, NRAS and HRAS) function as GDP-GTP-regulated binary on-off switches, which regulate cytoplasmic signaling networks that control diverse normal cellular processes. Gain-of-function missense mutations in RAS genes are found in ∼25% of human cancers, prompting interest in
Sònia Guil et al.
Cancer research, 63(17), 5178-5187 (2003-09-23)
We characterized a novel protein of the Ras family, p19 (H-RasIDX). The c-H-ras proto-oncogene undergoes alternative splicing of the exon termed IDX. We show that the alternative p19 mRNA is stable and as abundant as p21 (p21 H-Ras4A) mRNA in

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