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Key Documents

ST1099

Sigma-Aldrich

Anti-TORC2 (454-607) Rabbit pAb

liquid, Calbiochem®

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

antibody form

serum

antibody product type

primary antibodies

clone

polyclonal

form

liquid

does not contain

preservative

species reactivity

human, mouse, rat

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze

isotype

IgG

shipped in

wet ice

storage temp.

2-8°C

target post-translational modification

unmodified

General description

Rabbit polyclonal antibody supplied as undiluted serum. Recognizes the ~79-85 kDa TORC2 protein.
Recognizes the ~79-85 kDa TORC2 protein in primary hepatocytes, HepG2, NIH3T3, Min6, and FAO cells.
TORCs (Transducers Of Regulated cAMP Response Element-Binding (CREB) protein) are members of a conserved family of co-activators that enhance CRE-dependent transcription by a phosphorylation-independent interaction with the bZIP DNA binding/dimerization domain of CREB. Studies suggest that TORC phosphorylation and nuclear/cytoplasmic shuttling play an important role in the regulation of gluconeogenesis by cAMP.
This Anti-TORC2 (454-607) Rabbit pAb is validated for use in Immunoblotting, Immunoprecipitation for the detection of TORC2 (454-607).

Immunogen

Human
a recombinant protein consisting of amino acids 454-607 of mouse TORC2 fused to GST

Application


Immunoblotting (1:2000, see comments)
Immunoprecipitation (1:100, see comments)

Warning

Toxicity: Standard Handling (A)

Physical form

Undiluted serum.

Reconstitution

For long-term storage, aliquot and freeze (-20°C). In the case of storage at -20°C, avoid freeze/thaw cycles.

Analysis Note

Positive Control
Primary rat hepatocytes, HepG2, NIH3T3, Min6, and FAO cells

Other Notes

Screaton, R.A., et al. 2004. Cell119, 61.
This antibody has been used to detect endogenous TORC2 by immunoblotting. For immunoprecipitation, 4 µl antibody in a total volume of 400 µl has been tested. May also detect a protein at ~60 kDa, which may be a degradation product of TORC2. Antibody should be titrated for optimal results in individual systems.

Legal Information

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

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Storage Class

10 - Combustible liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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Haitao Wang et al.
Molecular endocrinology (Baltimore, Md.), 22(7), 1596-1605 (2008-05-10)
The transcriptional coactivator peroxisome-proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) is induced in the liver in response to fasting and coordinates the activation of targets necessary for increasing energy production for gluconeogenesis and ketogenesis. After partial hepatectomy, the liver must restore its mass
Julie A Highland et al.
American journal of physiology. Cell physiology, 307(7), C611-C621 (2014-08-01)
Entrainment of the intrinsic suprachiasmatic nucleus (SCN) molecular clock to the light-dark cycle depends on photic-driven intracellular signal transduction responses of SCN neurons that converge on cAMP response element-binding protein (CREB)-mediated regulation of gene transcription. Characterization of the CREB coactivator
Pablo E Hollstein et al.
Cancer discovery, 9(11), 1606-1627 (2019-07-28)
Mutations in the LKB1 (also known as STK11) tumor suppressor are the third most frequent genetic alteration in non-small cell lung cancer (NSCLC). LKB1 encodes a serine/threonine kinase that directly phosphorylates and activates 14 AMPK family kinases ("AMPKRs"). The function
John Le Lay et al.
Cell metabolism, 10(1), 55-62 (2009-07-09)
The liver contributes to glucose homeostasis by promoting either storage or production of glucose, depending on the physiological state. The cAMP response element-binding protein (CREB) is a principal regulator of genes involved in coordinating the hepatic response to fasting, but
Aijun Qiao et al.
The Journal of cell biology, 216(3), 723-741 (2017-02-12)
Metabolic energy reprogramming facilitates adaptations to a variety of stress conditions and cellular dysfunction, but how the energetic demands are monitored and met in response to physiological stimuli remains elusive. Our data support a model demonstrating that heat shock factor

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