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Principaux documents

M7570

Sigma-Aldrich

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

enhanced validation

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

Synonyme(s) :

Anti-MCOLN3, Anti-MLN3, Anti-TRPML3

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About This Item

Code UNSPSC :
12352203

Source biologique

rabbit

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen ~75 kDa

Espèces réactives

human

Validation améliorée

recombinant expression
Learn more about Antibody Enhanced Validation

Concentration

~1.5 mg/mL

Technique(s)

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

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

Description générale

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.

Immunogène

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.

Application

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

Actions biochimiques/physiologiques

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.

Forme physique

Solution in 0.01 M phosphate buffered saline, pH 7.4, and 15 mM sodium azide.

Clause de non-responsabilité

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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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

nwg

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Consulter la Bibliothèque de documents

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)
TRPML and lysosomal function
Zeevi DA, et al.
Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1772(8), 851-858 (2007)
Barbara Spix et al.
PloS one, 17(12), e0278848-e0278848 (2022-12-16)
TRPML3 (mucolipin 3, MCOLN3) is an endolysosomal cation channel belonging to the TRPML subfamily of transient receptor potential channels. Gain-of-function mutations in the Trpml3 gene cause deafness, circling behavior and coat color dilution in mice due to cell death of
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
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)

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