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Key Documents

SAB4200223

Sigma-Aldrich

Anti-phospho-TDP-43 [pSer409] antibody produced in rabbit

~1.0 mg/mL, affinity isolated antibody

Sinônimo(s):

Anti-phospho-ALS10, Anti-phospho-TAR DNA binding protein 43, Anti-phospho-TARDBP, Anti-phospho-TARDP43

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About This Item

Código UNSPSC:
12352203
NACRES:
NA.41

fonte biológica

rabbit

conjugado

unconjugated

forma do anticorpo

affinity isolated antibody

tipo de produto de anticorpo

primary antibodies

clone

polyclonal

forma

buffered aqueous solution

peso molecular

antigen ~43 kDa

reatividade de espécies

mouse, human

concentração

~1.0 mg/mL

técnica(s)

indirect immunofluorescence: 1-2 μg/mL using HeLa cells
western blot: 1-2 μg/mL using HepG2 and A431 cell lysates

nº de adesão UniProt

Condições de expedição

dry ice

temperatura de armazenamento

−20°C

modificação pós-traducional do alvo

phosphorylation (pSer409)

Informações sobre genes

human ... TARDBP(23435)
mouse ... Tardbp(230908)

Descrição geral

Transactive response DNA-binding protein 43 (TDP-43) belongs to the family of heterogeneous nuclear ribonucleoproteins (hnRNPs). It has two RNA-recognition motifs and a glycine-rich C-terminal sequence. TDP-43 is expressed in heart, lung, liver and brain, which is localized to the nucleus..

Imunogênio

synthetic peptide containing phosphorylated Ser409 of human TDP-43 conjugated to KLH. The corresponding sequence is identical in mouse TDP-43

Aplicação

Anti-phospho-TDP-43 [pSer409] antibody produced in rabbit has been used in:
  • enzyme linked immuno sorbent assay (ELISA)
  • immunohistochemistry
  • immunoblotting
  • immunofluorescence

Ações bioquímicas/fisiológicas

Transactive response DNA-binding protein 43 (TDP-43) binds to single stranded RNA. It regulates transcription regulation in human immunodeficiency virus (HIV). TDP-43 is the major ubiquinated component of cytoplasmic inclusions in frontotemporal lobe degeneration subtype (FTLD-U) and amyotrophic lateral sclerosis (ALS). Pathological TDP-43 forms abnormal inclusions in neuronal perikarya and neurites. Mutations in TDP-43 is associated with ALS. Abnormal phosphorylation of TDP-43 at Ser409/410 is observed in FTLD-U and ALS, leading to apoptosis.

forma física

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

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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Emily Feneberg et al.
Molecular neurobiology, 55(10), 7789-7801 (2018-02-21)
TDP-43 accumulates in nerve cells of nearly all cases of amyotrophic lateral sclerosis (ALS; the commonest form of motor neuron disease) and in the majority of Tau-negative frontotemporal lobar degeneration (FTLD). There is currently no biochemical test or marker of
TDP-43 mutations in familial and sporadic amyotrophic lateral sclerosis
Sreedharan J, et al.
Science (New York, N.Y.), 319(5870), 1668-1672 (2008)
Yuting Ren et al.
Frontiers in neurology, 12, 663637-663637 (2021-07-02)
Objective: The aim of this study was to measure both plasma and cerebrospinal fluid (CSF) TAR DNA-binding protein 43 (TDP-43) and phosphorylated TDP-43 (pTDP-43) levels in sporadic amyotrophic lateral sclerosis (sALS) patients, and to compare them with that of healthy
Towards a TDP-43-based biomarker for ALS and FTLD
Feneberg E, et al.
Molecular Neurobiology, 55(10), 7789-7801 (2018)
TDP-43-mediated neurodegeneration: towards a loss-of-function hypothesis?
Broeck LV, et al.
Trends in Molecular Medicine, 20(2), 66-71 (2014)

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