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ST1032

Sigma-Aldrich

Anti-TRB3 (1-145) Rabbit pAb

liquid, Calbiochem®

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About This Item

Código UNSPSC:
12352203
NACRES:
NA.41

origen biológico

rabbit

Nivel de calidad

forma del anticuerpo

serum

tipo de anticuerpo

primary antibodies

clon

polyclonal

Formulario

liquid

no contiene

preservative

reactividad de especies

rat, mouse, human

fabricante / nombre comercial

Calbiochem®

condiciones de almacenamiento

OK to freeze

isotipo

IgG

Condiciones de envío

wet ice

temp. de almacenamiento

2-8°C

modificación del objetivo postraduccional

unmodified

Información sobre el gen

human ... TRIB3(57761)

Descripción general

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).

Inmunógeno

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

Aplicación

Immunoblotting (1:2500)

Immunocytochemistry (1:2500)

Immunoprecipitation (1:250)

Advertencia

Toxicity: Standard Handling (A)

Forma física

Undiluted serum.

Reconstitución

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

Nota de análisis

Positive Control
HepG2 cells

Otras notas

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

Información legal

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

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Código de clase de almacenamiento

10 - Combustible liquids

Clase de riesgo para el agua (WGK)

WGK 1

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°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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