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Human TRIB3 Protein 2174

$300.00$1,000.00

Summary

  • Expression: Baculovirus-Insect Cells
  • Pure: Yes (SDS-PAGE)
  • Amino Acid Range: Met1-Gly358
SKU: 2174parent Categories: , Tag:
Weight1 lbs
Dimensions9 × 5 × 2 in
accession

Q96RU7

express system

Baculovirus-Insect Cells

product tag

N-GST

purity

> 90% as determined by Tris-Bis PAGE

background

Tribbles homolog 3 (TRIB3) is a mammalian gene that is upregulated in response to several types of cell death-inducing cellular stress. The TRIB3 protein is a pseudokinase, a protein kinase-like scaffold with impaired catalytic activity.

molecular weight

The protein has a predicted MW of 66.14 kDa same as Tris-Bis PAGE result.

available size

100 µg, 500 µg

endotoxin

Less than 1EU per μg by the LAL method.

Human TRIB3 Protein 2174

protein
Size and concentration
100, 500µg and liquid
Form
Liquid
Storage Instructions
Valid for 12 months from date of receipt when stored at -80°C. Recommend to aliquot the protein into smaller quantities for optimal storage. Please minimize freeze-thaw cycles.
Storage buffer
Shipped with dry ice.
Purity
> 95% as determined by Tris-Bis PAGE
target relevance
Tribbles homolog 3 (TRIB3) is a mammalian gene that is upregulated in response to several types of cell death-inducing cellular stress. The TRIB3 protein is a pseudokinase, a protein kinase-like scaffold with impaired catalytic activity.
Protein names
Tribbles homolog 3 (TRB-3) (Neuronal cell death-inducible putative kinase) (SINK) (p65-interacting inhibitor of NF-kappa-B)
Gene names
TRIB3,TRIB3 C20orf97 NIPK SKIP3 TRB3
Protein family
Protein kinase superfamily, CAMK Ser/Thr protein kinase family, Tribbles subfamily
Mass
9606Da
Function
Inactive protein kinase which acts as a regulator of the integrated stress response (ISR), a process for adaptation to various stress (PubMed:15775988, PubMed:15781252). Inhibits the transcriptional activity of DDIT3/CHOP and is involved in DDIT3/CHOP-dependent cell death during ER stress (PubMed:15775988, PubMed:15781252). May play a role in programmed neuronal cell death but does not appear to affect non-neuronal cells (PubMed:15775988, PubMed:15781252). Acts as a negative feedback regulator of the ATF4-dependent transcription during the ISR: while TRIB3 expression is promoted by ATF4, TRIB3 protein interacts with ATF4 and inhibits ATF4 transcription activity (By similarity). Disrupts insulin signaling by binding directly to Akt kinases and blocking their activation (By similarity). May bind directly to and mask the 'Thr-308' phosphorylation site in AKT1 (By similarity). Interacts with the NF-kappa-B transactivator p65 RELA and inhibits its phosphorylation and thus its transcriptional activation activity (PubMed:12736262). Interacts with MAPK kinases and regulates activation of MAP kinases (PubMed:15299019). Can inhibit APOBEC3A editing of nuclear DNA (PubMed:22977230).
Subellular location
Nucleus .
Tissues
Highest expression in liver, pancreas, peripheral blood leukocytes and bone marrow. Also highly expressed in a number of primary lung, colon and breast tumors. Expressed in spleen, thymus, and prostate and is undetectable in other examined tissues, including testis, ovary, small intestine, colon, leukocyte, heart, brain, placenta, lung, skeletal muscle, and kidney.
Structure
Interacts with AKT1, AKT2, MAP2K1 and MAP2K7 (PubMed:15299019). Interacts with ATF4 (PubMed:12743605). Interacts with DDIT3/CHOP and inhibits its interaction with EP300/P300 (PubMed:15775988, PubMed:17872950). Interacts with APOBEC3C (PubMed:22977230). Interacts (via N-terminus) with APOBEC3A (PubMed:22977230). Interacts with RELA (PubMed:12736262).
Domain
Th
Target Relevance information above includes information from UniProt accession: Q96RU7
The UniProt Consortium

SDS-PAGE gel of Human TRIB3 Protein
Human TRIB3 on Tris-Bis PAGE under reduced condition. The purity is greater than 90%.

Publications

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We haven't added any publications to our database yet.
Published literature highly relevant to the biological target of this product and referencing this antibody or clone are retrieved from PubMed database provided by The United States National Library of Medicine at the National Institutes of Health.

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