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Key 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

Synonym(s):

Anti-MCOLN3, Anti-MLN3, Anti-TRPML3

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About This Item

UNSPSC Code:
12352203

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~75 kDa

species reactivity

human

enhanced validation

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

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

General description

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.

Immunogen

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.

Biochem/physiol Actions

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.

Physical form

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

Disclaimer

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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Storage Class Code

10 - Combustible liquids

WGK

nwg

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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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