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Merck
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Key Documents

MABN473

Sigma-Aldrich

Anti-TMEM106B Antibody, clone TME-N 6F2

clone TME-N 6F2, from rat

Sinônimo(s):

Transmembrane protein 106B, TMEM106B

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About This Item

Código UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41

fonte biológica

rat

Nível de qualidade

forma do anticorpo

purified immunoglobulin

tipo de produto de anticorpo

primary antibodies

clone

TME-N 6F2, monoclonal

reatividade de espécies

rat, human

técnica(s)

immunofluorescence: suitable
western blot: suitable

nº de adesão NCBI

nº de adesão UniProt

Condições de expedição

wet ice

modificação pós-traducional do alvo

unmodified

Informações sobre genes

Descrição geral

Transmembrane protein 106B (TMEM106B) is a single-pass type II membrane protein present in endosomal and lysosomal membranes, and is highly expressed in the frontal cortex. Increased TMEM106B expression in the brain may be linked to mechanisms of disease in frontotemporal lobar degeneration with TAR DNA-binding protein (TDP-43) inclusions (FTLD-TDP). Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia.

Especificidade

This antibody recognizes the N-terminus of TMEM106B.

Imunogênio

Epitope: N-terminus
Recombinant protein corresponding to the N-terminus of human TMEM106B.

Aplicação

Anti-TMEM106B, clone TME-N 6F2 detects levels of TMEM106B proteins & has been published & validated for use in WB & IF.
Immunofluorescence Analysis: A 1:50 dilution from a representative lot detected TMEM106B in rat cerebellum tissue.
Research Category
Neuroscience
Research Sub Category
Neurodegenerative Diseases

Qualidade

Evaluated by Western Blot in human cortex tissue lysate.

Western Blot Analysis: 1 µg/mL of this antibody detected TMEM106B in 10 µg of human cortex tissue lysate.

Descrição-alvo

~30 kDa observed (At higher antibody concentrations, this protein may be observed at ~45 kDa). This protein may be observed at ~50 kDa due to glycosylation (Lang, C. M., et al. (2012). J Biol Chem. 287(23):19355-19365.).

forma física

Format: Purified
Protein G Purified
Purified rat monoclonal IgG2c in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Armazenamento e estabilidade

Stable for 1 year at 2-8°C from date of receipt.

Nota de análise

Control
Human cortex tissue lysate

Outras notas

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

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

12 - Non Combustible Liquids

Classe de risco de água (WGK)

WGK 1

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


Certificados de análise (COA)

Busque Certificados de análise (COA) digitando o Número do Lote do produto. Os números de lote e remessa podem ser encontrados no rótulo de um produto após a palavra “Lot” ou “Batch”.

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Christina M Lang et al.
The Journal of biological chemistry, 287(23), 19355-19365 (2012-04-19)
TMEM106B was identified as a major risk factor in a genome-wide association study for frontotemporal lobar degeneration (FTLD) with TAR DNA-binding protein (TDP)-43 pathology. The most significant association of TMEM106B single nucleotide polymorphisms with risk of FTLD-TDP was observed in
Benjamin M Schwenk et al.
The EMBO journal, 33(5), 450-467 (2013-12-21)
TMEM106B is a major risk factor for frontotemporal lobar degeneration with TDP-43 pathology. TMEM106B localizes to lysosomes, but its function remains unclear. We show that TMEM106B knockdown in primary neurons affects lysosomal trafficking and blunts dendritic arborization. We identify microtubule-associated
Common pathobiochemical hallmarks of progranulin-associated frontotemporal lobar degeneration and neuronal ceroid lipofuscinosis.
Gotzl, JK; Mori, K; Damme, M; Fellerer, K; Tahirovic, S; Kleinberger, G; Janssens et al.
Acta neuropathologica null

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