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Key Documents

T8076

Sigma-Aldrich

Anti-TRB-3 (N-terminal) antibody produced in rabbit

enhanced validation

affinity isolated antibody, buffered aqueous solution

Synonyme(s) :

Anti-Human tribbles 3 homolog, Anti-NIPK, Anti-SINK, Anti-SKIP3, Anti-TRIB3

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About This Item

Numéro MDL:
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.44

Source biologique

rabbit

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen 39 kDa

Espèces réactives

human

Validation améliorée

recombinant expression
Learn more about Antibody Enhanced Validation

Technique(s)

western blot: 1-2 μg/mL using HEK-293 cells expressing human TRB3

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 ... TRIB3(57761)

Description générale

Tribbles homolog 3 (TRB3) gene is located on the 20p13 human chromosome. TRB3 and its related family members TRB1 and TRB2 show 45% sequence identity. It exhibits resemblance to ′tribbles′, a drosophila protein. TRB family members have a truncated kinase domain that lacks an adenosine 5′-triphosphate binding site (GXGXXG) and contain a variant catalytic core motif.

Immunogène

synthetic peptide corresponding to amino acids 11-29 located near the N-terminus region of human TRB3. The immunizing sequence has limited homology (~50% identity) to mouse and rat TRB3, and has no identity to TRB1 and TRB2 isoforms.

Application

Anti-TRB3 (N-terminal) antibody produced in rabbit has been used in immunoprecipitation and immunoblotting.

Actions biochimiques/physiologiques

Tribbles homolog 3 (TRB3) like tribbles has also been identified as a potential pro-apoptotic protein, and is induced by a variety of cell stress conditions, including hypoxia and nutrient starvation. It was previously identified as a neuronal cell death-inducible protein kinase (NIPK) that is rapidly upregulated during neuronal apoptosis. TRB3 binds to activating transcription factor 4 (ATF4) and inhibits its transcriptional activity. TRB3 has been shown to interact with mitogen-activated protein kinases (MAPK) kinases to regulate activation of MAPK pathways.

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

Classe de danger pour l'eau (WGK)

WGK 3

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

TRB3: an oxidant stress-induced pseudokinase with a potential to negatively modulate MCP-1 cytokine in diabetic nephropathy
Kanwar YS
American Journal of Physiology: Renal Physiology, 299(5), F963-F964 (2010)
Downregulation of TRB3 protects neurons against apoptosis induced by global cerebral ischemia and reperfusion injury in rats
Wei K, et al.
Neuroscience, 360, 118-127 (2017)
Smyd1 facilitates heart development by antagonizing oxidative and ER stress responses
Rasmussen TL, et al.
PLoS ONE, 10(3), e0121765-e0121765 (2015)
CHOP10/TRB3/Akt signaling regulates ER stress apoptosis in colon cancer cells treated with prostamide-J
Albassam H, et al.
American Journal of Physiology: Renal Physiology (2019)
Zarka Sarwar et al.
The Journal of biological chemistry, 298(2), 101496-101496 (2021-12-19)
Deleted in Breast Cancer 1 (DBC1) is an important metabolic sensor. Previous studies have implicated DBC1 in various cellular functions, notably cell proliferation, apoptosis, histone modification, and adipogenesis. However, current reports about the role of DBC1 in tumorigenesis are controversial

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