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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

Código UNSPSC:
12352203
NACRES:
NA.41

origen biológico

rabbit

Nivel de calidad

conjugado

unconjugated

forma del anticuerpo

affinity isolated antibody

tipo de anticuerpo

primary antibodies

clon

polyclonal

Formulario

buffered aqueous solution

mol peso

antigen ~75 kDa

reactividad de especies

rat, mouse, human

envase

antibody small pack of 25 μL

validación mejorada

recombinant expression
Learn more about Antibody Enhanced Validation

concentración

~1.5 mg/mL

técnicas

western blot: 0.5-1 μg/mL using HEK-293T cells expressing human mucolipin-3

Nº de acceso UniProt

Condiciones de envío

dry ice

temp. de almacenamiento

−20°C

modificación del objetivo postraduccional

unmodified

Información sobre el gen

Descripción general

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.

Especificidad

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

Inmunógeno

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

Aplicación

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

Acciones bioquímicas o fisiológicas

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.

Forma física

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

Cláusula de descargo de responsabilidad

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 clase de almacenamiento

10 - Combustible liquids

Clase de riesgo para el agua (WGK)

nwg

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable

Equipo de protección personal

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


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Certificados de análisis (COA)

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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 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)
The regulatory mechanism of mammalian TRPML s revealed by cryo-EM
Schmiege P, et al.
FEBS Journal, 285(14), 2579-2585 (2018)
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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