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Merck

M1071

Sigma-Aldrich

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

enhanced validation

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

Sinónimos:

Anti-MCOLN3, Anti-MLN3, Anti-TRPML3

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

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

rat, mouse, human

packaging

antibody small pack of 25 μL

enhanced validation

recombinant expression
Learn more about Antibody Enhanced Validation

concentration

~1.5 mg/mL

technique(s)

western blot: 0.5-1 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 (MLN3) belongs to mucolipin subfamily. It consists of six transmembrane domain (TMD), with a putative pore region between TMD5 and TMD6 and cytosolic N- and C-termini. MLN3 is a Ca2+ permeable cation channel, which is expressed in the plasma membrane, endosomes, lysosomes and autophagosomes.

Specificity

Additional bands may be observed at ~150 kDa and ~50 kDa due to aggregation and degradation, respectively.

Immunogen

synthetic peptide corresponding to amino acids 529-542 of human mucolipin-3. This sequence is identical in mouse and rat mucoplipin-3.

Application

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

Biochem/physiol Actions

Mucolipin-3 (MLN3) regulates endocytic pathway and lysosomal integrity. It modulates membrane trafficking and autophagy. Abnormalities of transient receptor potential cation channel, mucolipin subfamily, member 3 (TRPML3) are linked to early deafness, pigmentation abnormalities, and perinatal lethality in mice. Mutations in mouse mucolipin-3 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

10 - Combustible liquids

wgk_germany

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Visite la Librería de documentos

Heteromultimeric TRPML channel assemblies play a crucial role in the regulation of cell viability models and starvation-induced autophagy
Zeevi DA, et al.
Journal of Cell Science, 123(18), 3112-3124 (2010)
Emmanuel Gonzales et al.
Journal of hepatology, 52(1), 54-62 (2009-11-17)
Paracrine interactions are critical to liver physiology, particularly during regeneration, although physiological involvement of extracellular ATP, a crucial intercellular messenger, remains unclear. The physiological release of ATP into extracellular milieu and its impact on regeneration after partial hepatectomy were investigated
The regulatory mechanism of mammalian TRPML s revealed by cryo-EM
Schmiege P, et al.
FEBS Journal, 285(14), 2579-2585 (2018)
The Ca2+ channel TRPML3 specifically interacts with the mammalian ATG8 homologue GATE16 to regulate autophagy
Choi S and Kim HJ
Biochemical and Biophysical Research Communications, 443(1), 56-61 (2014)
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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