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M7570

Sigma-Aldrich

Anti-Mucolipin-3 (N-terminal) antibody produced in rabbit

enhanced validation

~1.5 mg/mL, affinity isolated antibody, buffered aqueous solution

Sinônimo(s):

Anti-MCOLN3, Anti-MLN3, Anti-TRPML3

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About This Item

Código UNSPSC:
12352203

fonte biológica

rabbit

conjugado

unconjugated

forma do anticorpo

affinity isolated antibody

tipo de produto de anticorpo

primary antibodies

clone

polyclonal

Formulário

buffered aqueous solution

peso molecular

antigen ~75 kDa

reatividade de espécies

human

validação aprimorada

recombinant expression
Learn more about Antibody Enhanced Validation

concentração

~1.5 mg/mL

técnica(s)

western blot: 0.25-0.5 μg/mL using HEK-293T cells expressing human mucolipin-3

nº de adesão UniProt

Condições de expedição

dry ice

temperatura de armazenamento

−20°C

modificação pós-traducional do alvo

unmodified

Informações sobre genes

Descrição geral

Mucolipin 3 (MCOLN3) belongs to the mucolipin family of ion channels and the superfamily of transient receptor potential (TRP) channels. This 553-amino acid protein is expressed in the early and late endosomes of epithelial cells. MCOLN3 possesses six transmembrane domains with the tails oriented towards the interior the cytosol.
Mucolipin-3 is mapped to human chromosome 1p22.3.

Imunogênio

synthetic peptide corresponding to amino acids 26-43 of human mucolipin-3. This sequence is identical between human and mouse and highly conserved in mouse and rat.

Aplicação

Anti-Mucolipin-3 (N-terminal) antibody produced in rabbit
has been used in immunoblotting and immunostaining.

Ações bioquímicas/fisiológicas

Mucolipin 3 (MCOLN3) is a Ca2+-permeable channel which regulates the cargo traffic along the endosomal pathway. Its activity is regulated by changes in the pH. Overexpression of MCOLN3 in cells lead to large variations in the endosomal pathway and the depletion in its levels leads to the degradation of the epidermal growth factor receptor (EGFR).
Mutations in mouse mucolipin3 (MLN3, TRPML3) encoded by the MCOLN3 gene, are associated with deafness and pigmentation defects in varitint-waddler mice.

forma física

Solution in 0.01 M phosphate buffered saline, pH 7.4, and 15 mM 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)

nwg

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


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Visite a Biblioteca de Documentos

TRPML and lysosomal function
Zeevi DA, et al.
Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1772(8), 851-858 (2007)
Expression and vesicular localization of mouse Trpml3 in stria vascularis, hair cells, and vomeronasal and olfactory receptor neurons
Castiglioni AJ, et al.
The Journal of Comparative Neurology, 519(6), 1095-1114 (2011)
Andrew J Castiglioni et al.
The Journal of comparative neurology, 519(6), 1095-1114 (2011-02-24)
TRPML3 is a member of the mucolipin branch of the transient receptor potential cation channel family. A dominant missense mutation in Trpml3 (also known as Mcoln3) causes deafness and vestibular impairment characterized by stereocilia disorganization, hair cell loss, and endocochlear
Mutations in Mcoln3 associated with deafness and pigmentation defects in varitint-waddler (Va) mice
Di Palma F, et al.
Proceedings of the National Academy of Sciences of the USA, 99(23), 14994-14999 (2002)
Jose A Martina et al.
Traffic (Copenhagen, Denmark), 10(8), 1143-1156 (2009-06-06)
The varitint-waddler phenotype in mice is caused by gain-of-function mutations in mucolipin-3 (MCOLN3), a member of the mucolipin family of ion channels. These mice are characterized by defects in pigmentation, hearing loss and vestibular defects, suggesting that MCOLN3 might play

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