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Merck

SAB1405964

Sigma-Aldrich

Anti-HRAS antibody produced in mouse

purified immunoglobulin, buffered aqueous solution

Synonym(e):

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

Biologische Quelle

mouse

Konjugat

unconjugated

Antikörperform

purified immunoglobulin

Antikörper-Produkttyp

primary antibodies

Klon

polyclonal

Form

buffered aqueous solution

Mol-Gew.

antigen ~20.79 kDa

Speziesreaktivität

human

Methode(n)

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

NCBI-Hinterlegungsnummer

UniProt-Hinterlegungsnummer

Versandbedingung

dry ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

human ... HRAS(3265)

Allgemeine Beschreibung

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

Anwendung

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

Biochem./physiol. Wirkung

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.

Physikalische Form

Solution in phosphate buffered saline, pH 7.4

Haftungsausschluss

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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Lagerklassenschlüssel

10 - Combustible liquids

WGK

WGK 1

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


Analysenzertifikate (COA)

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Die Dokumentenbibliothek aufrufen

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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