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Merck

371729

Anti-Giα-3-Subunit, C-Terminal (345-354) Rabbit pAb

liquid, Calbiochem®

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제품정보 (DICE 배송 시 비용 별도)

NACRES:
NA.43
UNSPSC Code:
12352203
Clone:
polyclonal
Species reactivity:
-
Application:
Citations:
13
기술 서비스
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도움 문의
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도움 문의

biological source

rabbit

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

liquid

does not contain

preservative

species reactivity (predicted by homology)

mammals

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze, avoid repeated freeze/thaw cycles

dilution

(Immunoblotting (1:1000)
Immunoprecipitation )

isotype

IgG

shipped in

wet ice

storage temp.

−70°C

target post-translational modification

unmodified

Quality Level

Gene Information

human ... GNAI3(2773)

General description

Anti-Giα-3-Subunit, C-Terminal (345-354), rabbit polyclonal, recognizes Giα-3 subunit. Does not cross-react with Gsα & Goα subunits. Validated for use in WB & IP.
Immunoaffinity purified rabbit polyclonal antibody. Recognizes the Giα-3 subunit protein.
Recognizes Giα-3 subunit. Does not cross-react with Gsα and Goα, but partially cross-reacts with Giα1-, G1α2-subunits.

Immunogen

a synthetic peptide (CKNNLKECGLY) corresponding to amino acids at the C-terminus of mammalian Giα-3, conjugated to KLH

Application

Immunoblotting (1:1000)

Immunoprecipitation (see comments)

Physical form

In 140 mM NaCl, 100 mM potassium phosphate, pH 7.5.

Preparation Note

Following initial thaw, aliquot and freeze (-20°C).

Other Notes

Kumar, R., et al. 1994. J. Mol. Cell. Cardiol. 26, 1537.
Raymond, J.R., et al. 1993. Biochemistry32, 11064.
Mumby, S.M., and Gilman, A.G. 1991. Methods Enzymol.195, 215.
Jones, D.T., and Reed, R.R. 1987. J. Biol. Chem.262, 14,241.
The specificity was confirmed with lysates from separate cultures of bacteria transfected with the genes for Gsα, Giα-1, GIα-2, Giα-3, and Goα. The original titer of the serum was 1:10,000. Suitable for immunoblotting and immunoprecipitation. Does not cross-react with Gsα and Goα. Antibody partially cross-reacts with Giα-1 and GIα-2. Variables associated with assay conditions will dictate the proper working dilution.

Legal Information

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

Disclaimer

Toxicity: Standard Handling (A)

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저장 등급

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


시험 성적서(COA)

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문서 라이브러리에서 최근에 구매한 제품에 대한 문서를 찾아보세요.

문서 라이브러리 방문

R R Mirotznik et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 20(20), 7614-7621 (2000-10-12)
The inhibition of presynaptic calcium channels via G-protein-dependent second messenger pathways is a key mechanism of transmitter release modulation. We used the calyx-type nerve terminal of the chick ciliary ganglion to examine which G-proteins are involved in the voltage-sensitive inhibition
C Chen
The American journal of physiology, 275(2), E278-E284 (1998-08-04)
Voltage-gated K+ currents in rat somatotrophs are increased by somatostatin (SRIF) through unidentified G protein. In this experiment, somatotroph-enriched cells (up to 85%) were obtained from ovine pituitary glands and further identified by the increase in K+ currents by SRIF.
Heng Xu et al.
Brain research bulletin, 77(1), 49-54 (2008-07-22)
Recent evidence indicates that agonist ligands of G protein coupled receptors (GPCR) can activate different signaling systems. Such "agonist-directed" signaling also occurs with opioid receptors. Previous work from our laboratory showed that chronic morphine, but not DAMGO, up-regulates the expression
C Chen et al.
The Journal of physiology, 491 ( Pt 1), 21-29 (1996-02-15)
1. Somatotroph-enriched cells (up to 85%) were obtained from ovine pituitary glands by means of collagenase dissociation and Percoll-gradient centrifugation. Further identification was based on the reduction in Ca2+ currents by 10 nM somatostatin (SRIF). 2. The whole-cell configuration of
Jun Cheng et al.
American journal of physiology. Heart and circulatory physiology, 302(7), H1454-H1465 (2012-01-31)
Calmodulin-dependent protein kinase II (CaMKII) has been proposed to be a therapeutic target for heart failure (HF). However, the cardiac effect of chronic CaMKII inhibition in HF has not been well understood. We have tested alterations of Ca(2+) handling, excitation-contraction

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SKUGTIN
371729-50ULCN04055977213300

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