Direkt zum Inhalt
Merck
Alle Fotos(1)

Key Documents

ST1032

Sigma-Aldrich

Anti-TRB3 (1-145) Rabbit pAb

liquid, Calbiochem®

Anmeldenzur Ansicht organisationsspezifischer und vertraglich vereinbarter Preise


About This Item

UNSPSC-Code:
12352203
NACRES:
NA.41

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)

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

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

Sie haben nicht das passende Produkt gefunden?  

Probieren Sie unser Produkt-Auswahlhilfe. aus.

Lagerklassenschlüssel

10 - Combustible liquids

WGK

WGK 1

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


Analysenzertifikate (COA)

Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.

Besitzen Sie dieses Produkt bereits?

In der Dokumentenbibliothek finden Sie die Dokumentation zu den Produkten, die Sie kürzlich erworben haben.

Die Dokumentenbibliothek aufrufen

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

Unser Team von Wissenschaftlern verfügt über Erfahrung in allen Forschungsbereichen einschließlich Life Science, Materialwissenschaften, chemischer Synthese, Chromatographie, Analytik und vielen mehr..

Setzen Sie sich mit dem technischen Dienst in Verbindung.