SAB5300028
Monoclonal Anti-RAB10 antibody produced in mouse
clone 4E2, ascites fluid
Sinônimo(s):
RAB10
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About This Item
Código UNSPSC:
12352203
NACRES:
NA.41
conjugado:
unconjugated
application:
ELISA (d)
IF
WB
IF
WB
clone:
4E2, monoclonal
reatividade de espécies:
mouse, human
citations:
12
técnica(s):
direct ELISA: 1:10,000
indirect immunofluorescence: 1:200-1:1,000
western blot: 1:500-1:2,000
indirect immunofluorescence: 1:200-1:1,000
western blot: 1:500-1:2,000
Produtos recomendados
fonte biológica
mouse
Nível de qualidade
conjugado
unconjugated
forma do anticorpo
ascites fluid
tipo de produto de anticorpo
primary antibodies
clone
4E2, monoclonal
peso molecular
22.5 kDa
reatividade de espécies
mouse, human
técnica(s)
direct ELISA: 1:10,000
indirect immunofluorescence: 1:200-1:1,000
western blot: 1:500-1:2,000
Isotipo
IgG1
nº de adesão NCBI
nº de adesão UniProt
Condições de expedição
wet ice
temperatura de armazenamento
−20°C
modificação pós-traducional do alvo
unmodified
Informações sobre genes
human ... Rab10(10890)
Descrição geral
Rab10, a small monomeric Ras-related GTP-binding protein, is a member of the rat sarcoma (RAS) family. RAB10 gene has GTP and GDP binding domains. RAB10 gene is located on human chromosome 2p23.3.
Imunogênio
Purified recombinant fragment of human Rab10 expressed in E.coli.
Mouse monoclonal antibody raised against Rab10
Mouse monoclonal antibody raised against Rab10
Aplicação
Monoclonal Anti-RAB10 antibody produced in mouse has been used in western blotting (1:1000) and immunocytochemistry (1:1000).
Ações bioquímicas/fisiológicas
RAB10 is involved in intracellular vesicle trafficking. It is important for insulin-stimulated glucose transporter type 4 (GLUT4) translocation in adipocytes, the secretion of the basement membrane, and endoplasmic reticulum development and maintenance (ER). It controls toll-like receptor 4 (TLR4) trafficking, which is crucial for innate immune responses. Rab10 gene knockdown reduces the production of Aβ and higher expression of Rab10 enhances amyloid β protein (Aβ) production in cultured neuroblastoma cells. Phosphorylation of Rab10 could be the cause of vesicle trafficking abnormalities that lead to neurodegeneration in Alzheimer′s disease. Overexpression of RAB10 is observed in hepatocellular carcinoma (HCC).
forma física
Ascitic fluid containing 0.03% sodium azide.
Exoneração de responsabilidade
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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Código de classe de armazenamento
10 - Combustible liquids
Classe de risco de água (WGK)
WGK 3
Ponto de fulgor (°F)
Not applicable
Ponto de fulgor (°C)
Not applicable
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RAB10 overexpression promotes tumor growth and indicates poor prognosis of hepatocellular carcinoma.
Wei Wang et al.
Oncotarget, 8(16), 26434-26447 (2017-05-04)
Hepatocellular carcinoma (HCC), one of the most common and lethal cancers worldwide, has a high recurrence rate with current treatment modalities. Identifying biomarkers for early diagnosis and discovering new sufficient molecular targets for the development of targeted therapies are urgently
Shea J Andrews et al.
Current genetic medicine reports, 7(1), 1-12 (2019-03-01)
Over the last decade over 40 loci have been associated with risk of Alzheimer's disease (AD). However, most studies have either focused on identifying risk loci or performing unbiased screens without a focus on protective variation in AD. Here, we
Andrew J Lindsay et al.
Molecular biology of the cell, 24(21), 3420-3434 (2013-09-06)
Myosin Va is a widely expressed actin-based motor protein that binds members of the Rab GTPase family (3A, 8A, 10, 11A, 27A) and is implicated in many intracellular trafficking processes. To our knowledge, myosin Va has not been tested in
Elena Fdez et al.
iScience, 25(6), 104476-104476 (2022-06-21)
Mutations in LRRK2 increase its kinase activity and cause Parkinson's disease. LRRK2 phosphorylates a subset of Rab proteins which allows for their binding to RILPL1. The phospho-Rab/RILPL1 interaction causes deficits in ciliogenesis and interferes with the cohesion of duplicated centrosomes.
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