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Documentos Principais

ST1032

Sigma-Aldrich

Anti-TRB3 (1-145) Rabbit pAb

liquid, Calbiochem®

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About This Item

Código UNSPSC:
12352203
NACRES:
NA.41

fonte biológica

rabbit

Nível de qualidade

forma do anticorpo

serum

tipo de produto de anticorpo

primary antibodies

clone

polyclonal

Formulário

liquid

não contém

preservative

reatividade de espécies

rat, mouse, human

fabricante/nome comercial

Calbiochem®

condição de armazenamento

OK to freeze

Isotipo

IgG

Condições de expedição

wet ice

temperatura de armazenamento

2-8°C

modificação pós-traducional do alvo

unmodified

Informações sobre genes

human ... TRIB3(57761)

Descrição geral

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).

Imunogênio

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

Aplicação

Immunoblotting (1:2500)

Immunocytochemistry (1:2500)

Immunoprecipitation (1:250)

Advertência

Toxicity: Standard Handling (A)

forma física

Undiluted serum.

Reconstituição

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

Nota de análise

Positive Control
HepG2 cells

Outras notas

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

Informações legais

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

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Código de classe de armazenamento

10 - Combustible liquids

Classe de risco de água (WGK)

WGK 1

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°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
Ran Hee Choi et al.
Biochemical and biophysical research communications, 493(3), 1236-1242 (2017-10-01)
Skeletal muscle atrophy is associated with a disruption in protein turnover involving increased protein degradation and suppressed protein synthesis. Although it has been well studied that the IGF-1/PI3K/Akt pathway plays an essential role in the regulation of the protein turnover
Pascaline Aimé et al.
Neurobiology of disease, 136, 104725-104725 (2020-01-09)
Identifying disease-causing pathways and drugs that target them in Parkinson's disease (PD) has remained challenging. We uncovered a PD-relevant pathway in which the stress-regulated heterodimeric transcription complex CHOP/ATF4 induces the neuron prodeath protein Trib3 that in turn depletes the neuronal
Saravanan S Karuppagounder et al.
Science translational medicine, 8(328), 328ra29-328ra29 (2016-03-05)
Disability or death due to intracerebral hemorrhage (ICH) is attributed to blood lysis, liberation of iron, and consequent oxidative stress. Iron chelators bind to free iron and prevent neuronal death induced by oxidative stress and disability due to ICH, but

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