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Key Documents

SAB1405964

Sigma-Aldrich

Anti-HRAS antibody produced in mouse

purified immunoglobulin, buffered aqueous solution

Sinonimo/i:

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

Codice UNSPSC:
12352203
NACRES:
NA.41

Origine biologica

mouse

Coniugato

unconjugated

Forma dell’anticorpo

purified immunoglobulin

Tipo di anticorpo

primary antibodies

Clone

polyclonal

Forma fisica

buffered aqueous solution

PM

antigen ~20.79 kDa

Reattività contro le specie

human

tecniche

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

N° accesso NCBI

N° accesso UniProt

Condizioni di spedizione

dry ice

Temperatura di conservazione

−20°C

modifica post-traduzionali bersaglio

unmodified

Informazioni sul gene

human ... HRAS(3265)

Descrizione generale

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.

Immunogeno

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

Sequence
MTEYKLVVVGAGGVGKSALTIQLIQNHFVDEYDPTIEDSYRKQVVIDGETCLLDILDTAGQEEYSAMRDQYMRTGEGFLCVFAINNTKSFEDIHQYREQIKRVKDSDDVPMVLVGNKCDLAARTVESRQAQDLARSYGIPYIETSAKTRQGVEDAFYTLVREIRQHKLRKLNPPDESGPGCMSCKCVLS

Applicazioni

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

Azioni biochim/fisiol

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.

Stato fisico

Solution in phosphate buffered saline, pH 7.4

Esclusione di responsabilità

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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Codice della classe di stoccaggio

10 - Combustible liquids

Classe di pericolosità dell'acqua (WGK)

WGK 1

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


Certificati d'analisi (COA)

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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
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
Tushar Gupta et al.
Journal of virology, 89(9), 5124-5133 (2015-02-27)
The E2F family of transcription factors, broadly divided into activator and repressor E2Fs, regulates cell cycle genes. Current models indicate that activator E2Fs are necessary for cell cycle progression and tumorigenesis and are also required to mediate transformation induced by
Jie Song et al.
Oncology reports, 31(6), 2776-2784 (2014-04-05)
R-Ras, a member of the Ras superfamily, is expressed in a wide variety of tissues and regulates cell adhesion, migration, differentiation and apoptosis. Research has raised the possibility that R-Ras may function as a positive regulator of cell proliferation and

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