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ST1032

Sigma-Aldrich

Anti-TRB3 (1-145) Rabbit pAb

liquid, Calbiochem®

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biological source

rabbit

Quality Level

antibody form

serum

antibody product type

primary antibodies

clone

polyclonal

form

liquid

does not contain

preservative

species reactivity

rat, mouse, human

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze

isotype

IgG

shipped in

wet ice

storage temp.

2-8°C

target post-translational modification

unmodified

Gene Information

human ... TRIB3(57761)

General description

Rabbit polyclonal antibdy supplied as undiluted serum that has been adsorbed against GST to remove GST-reactive antibodies. Recognizes the ~45 kDa TRB3 protein.
Recognizes the ~45 kDa TRB3 protein in HepG2 cells.
TRB3 is a protein that is reported to disrupt insulin signaling by binding directly to Akt and blocking activation of the kinase.
This Anti-TRB3 (1-145) Rabbit pAb is validated for use in Immunoblotting, Immunocytochemistry, Immunoprecipitation for the detection of TRB3 (1-145).

Immunogen

Mouse
a recombinant protein consisting of amino acids 1-145 of mouse TRB3, fused to GST

Application

Immunoblotting (1:2500)

Immunocytochemistry (1:2500)

Immunoprecipitation (1:250)

Warning

Toxicity: Standard Handling (A)

Physical form

Undiluted serum.

Reconstitution

For long-term storage aliquot and freeze (-20°C). Avoid freeze/thaw cycles.

Analysis Note

Positive Control
HepG2 cells

Other Notes

Antibody should be titrated for optimal results in individual systems.
Du, K., et al. 2003. Science300, 1574.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class Code

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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N Zareen et al.
Cell death and differentiation, 20(12), 1719-1730 (2013-11-12)
The mechanisms governing neuron death following NGF deprivation are incompletely understood. Here, we show that Trib3, a protein induced by NGF withdrawal, has a key role in such death via a loop involving the survival kinase Akt and FoxO transcription
Wei Luo et al.
Frontiers in physiology, 12, 637432-637432 (2021-06-29)
Eccentric exercise training accompanied by a low-fat diet can prevent insulin resistance (IR) and is currently an effective method for the treatment of IR induced by high-fat diet (HFD)-associated obesity. However, the molecular mechanisms underlying this improvement of IR in
Bevin C English et al.
PLoS pathogens, 13(9), e1006589-e1006589 (2017-09-28)
The ability of intracellular pathogens to manipulate host-cell viability is critical to successful infection. Some pathogens promote host-cell survival to protect their replicative niche, whereas others trigger host-cell death to facilitate release and dissemination of the pathogen after intracellular replication
Tiit Örd et al.
Cancers, 13(10) (2021-06-03)
The proteasome is an appealing target for anticancer therapy and the proteasome inhibitor bortezomib has been approved for the treatment of several types of malignancies. However, the molecular mechanisms underlying cancer cell resistance to bortezomib remain poorly understood. In the
Viviana M Berthoud et al.
The Journal of biological chemistry, 291(34), 17569-17578 (2016-06-19)
Mice expressing connexin50D47A (Cx50D47A) exhibit nuclear cataracts and impaired differentiation. Cx50D47A does not traffic properly, and homozygous mutant lenses show increased levels of the stress-responsive αB-crystallins. Therefore, we assessed whether expression of Cx50D47A led to endoplasmic reticulum (ER) stress in

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