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Key Documents

SAB4200006

Sigma-Aldrich

Anti-TDP-43 (N-terminal region) antibody produced in rabbit

~1.0 mg/mL, affinity isolated antibody, buffered aqueous solution

Synonyme(s) :

Anti-ALS10, Anti-TARDBP, Anti-TARDP43, Anti-Tar DNA binding protein 43

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen ~43 kDa

Espèces réactives

mouse, human

Concentration

~1.0 mg/mL

Technique(s)

immunohistochemistry: 5-10 μg/mL using human or mouse kidney
indirect immunofluorescence: 5-10 μg/mL using HepG2 cells
western blot: 1.5-3.0 μg/mL using HepG2 cell lysates

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

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

Description générale

TDP-43 (TAR DNA binding protein, TARDP) belongs to the family of heterogeneous nuclear ribonucleoproteins (hnRNPs) that bind single stranded RNA. TDP-43 is predominantly localized to the nucleus.

Application

Anti-TDP-43 (N-terminal region) antibody produced in rabbit has been used in:
  • immunoblotting
  • immunofluorescence
  • immunohistochemistry
  • immunuprecipitation

Actions biochimiques/physiologiques

TDP-43 is also involved in mediating the transcription regulation of human immune deficiency virus (HIV). TDP-43 has been identified as 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, indicating that redistribution of TDP-43 to the cytoplasm is a pathogenic mechanism. Several pathogenic TDP43 mutations have been identified in familial ALS, causing aberrant cleavage of TDP-43 to C-terminal fragments, and predisposing nuclear TDP-43 to redistribute to the cytoplasm and form pathological aggregates. Abnormal phosphorylation of TDP-43 at Ser409/410 has also been observed in frontotemporal lobar degeneration and amyotrophic lateral sclerosis (FTLD-U and ALS) suggesting a toxic gain of function leading to apoptosis.

Forme physique

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

Clause de non-responsabilité

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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Code de la classe de stockage

10 - Combustible liquids

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

TDP-43 deposition in prospectively followed, cognitively normal elderly individuals: correlation with argyrophilic grains but not other concomitant pathologies
Arnold, Stacy J and Dugger, Brittany N and Beach, Thomas G
Acta Neuropathologica, 126(1), 51-57 (2013)
TDP-43 loss of function inhibits endosomal trafficking and alters trophic signaling in neurons
Schwenk BM, et al.
The Embo Journal, 35(21), 2350-2370 (2016)
Aberrant cleavage of TDP-43 enhances aggregation and cellular toxicity
Zhang YJ, et al.
Proceedings of the National Academy of Sciences of the USA, 106(18), 7607-7612 (2009)
Cross-regulation between TDP-43 and paraspeckles promotes pluripotency-differentiation transition
Modic M, et al.
Molecular Cell (2019)
Carlo Scialò et al.
Brain communications, 2(2), fcaa142-fcaa142 (2020-10-24)
The pathological deposition of the transactive response DNA-binding protein of 43 kDa occurs in the majority (∼97%) of amyotrophic lateral sclerosis and in around 45% of frontotemporal lobar degeneration cases. Amyotrophic lateral sclerosis and frontotemporal lobar degeneration clinically overlap, presenting a

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