ST1032
Anti-TRB3 (1-145) Rabbit pAb
liquid, Calbiochem®
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About This Item
UNSPSC-Code:
12352203
NACRES:
NA.41
Empfohlene Produkte
Biologische Quelle
rabbit
Qualitätsniveau
Antikörperform
serum
Antikörper-Produkttyp
primary antibodies
Klon
polyclonal
Form
liquid
Enthält nicht
preservative
Speziesreaktivität
rat, mouse, human
Hersteller/Markenname
Calbiochem®
Lagerbedingungen
OK to freeze
Isotyp
IgG
Versandbedingung
wet ice
Lagertemp.
2-8°C
Posttranslationale Modifikation Target
unmodified
Angaben zum Gen
human ... TRIB3(57761)
Allgemeine Beschreibung
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
Anwendung
Immunoblotting (1:2500)
Immunocytochemistry (1:2500)
Immunoprecipitation (1:250)
Immunocytochemistry (1:2500)
Immunoprecipitation (1:250)
Warnhinweis
Toxicity: Standard Handling (A)
Physikalische Form
Undiluted serum.
Rekonstituierung
For long-term storage aliquot and freeze (-20°C). Avoid freeze/thaw cycles.
Hinweis zur Analyse
Positive Control
HepG2 cells
HepG2 cells
Sonstige Hinweise
Antibody should be titrated for optimal results in individual systems.
Du, K., et al. 2003. Science300, 1574.
Rechtliche Hinweise
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
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Lagerklassenschlüssel
10 - Combustible liquids
WGK
WGK 1
Flammpunkt (°F)
Not applicable
Flammpunkt (°C)
Not applicable
Analysenzertifikate (COA)
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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
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
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
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
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
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