Rabbit Anti-Human CCKAR (a.a. 161-200) Polyclonal antibody

Name: Rabbit Anti-Human CCKAR (a.a. 161-200) Polyclonal antibody
SKU: DPABH-02465
Rating: 5 (1 reviews)

Rabbit Anti-Human CCKAR (a.a. 161-200) Polyclonal antibody for WB

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COA

SDS

Datasheet

Key features and details

Target: CCKAR
Host: Rabbit
Application: WB
Species Reactivity: Human, Mouse, Rat, Chicken, Dog, Pig, Cow, Horse, Sheep, Goat

Summary

Specifications

Antibody Isotype

IgG

Species Reactivity

Human; Mouse; Rat; Chicken; Dog; Pig; Cow; Horse; Sheep; Goat

Immunogen

KLH conjugated synthetic peptide derived from human CCKAR: 161-200/428

Conjugate

Unconjugated

Applications

Application Notes

WB: 1:500-2000

General Notes

This product (Catalog No. DPABH-02465) is a rabbit-derived IgG polyclonal antibody raised against human CCKAR, targeting the amino acid region 161–200 of the protein. This antibody exhibits cross-reactivity with CCKAR from mouse, rat, chicken, dog, pig, cow, horse, sheep, and goat. It has been affinity purified by Protein A. This gene encodes a G-protein coupled receptor that binds non-sulfated members of the cholecystokinin (CCK) family of peptide hormones. This receptor is a major physiologic mediator of pancreatic enzyme secretion and smooth muscle contraction of the gallbladder and stomach. In the central and peripheral nervous system this receptor regulates satiety and the release of beta-endorphin and dopamine.
DPABH-02465 is suitable for use in Western blot (WB) (1:500–1:2,000) application.
DPABH-02465 is supplied as a liquid formulation in 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. For long-term storage, keep at −20 °C. For short-term use, store at 2–8 °C. Avoid repeated freeze–thaw cycles to maintain antibody integrity and performance.

Target

Alternative Names

CCK A; CCK A receptor; CCK AR; CCK-AR; CCKAR_HUMAN

Entrez Gene ID

886

UniProt ID

P32238

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Exocrine pancreatic insufficiency in the Eurasian dog breed - inheritance and exclusion of two candidate genes

ANIMAL GENETICS

Authors: Proschowsky, H. F.; Fredholm, M.

Abstract

Exocrine pancreatic insufficiency is considered an inherited disease in several dog breeds. Affected dogs show polyphagia, weight loss and voluminous faeces of light colour due to the lack of pancreatic enzymes. In the study described herein, we performed a segregation analysis using the SINGLES method for three families of the Eurasian dog breed. Our data were consistent with an autosomal recessive mode of inheritance. In addition, we performed a linkage analysis in these families using four microsatellite markers on CFA3 and two microsatellites on CFA23. Based on our results, we excluded the canine orthologs of the human cholecystokinin (CCK) and the cholecystokinin A receptor (CCKAR) genes as candidates for exocrine pancreatic insufficiency.

Disrupted cholecystokinin type-A receptor (CCKAR) gene in OLETF rats

GENE

Authors: Takiguchi, S; Takata, Y; Funakoshi, A; Miyasaka, K; Kataoka, K; Fujimura, Y; Goto, T; Kono, A

Abstract

OLETF rats develop hyperglycemia, hyperinsulinemia and mild obesity, which is characteristic of human non-insulin-dependent diabetes mellitus (NIDDM). We cloned and sequenced the cholecystokinin type-A receptor (CCKAR) gene in the rats. Comparing the DNA sequences of the OLETF CCKAR gene and LETO CCKAR gene, normal gene, we found a deletion in the OLETF gene, 6847 bases in length, which was flanked by two 3-base-pair direct repeats (5'-TGT-3') at positions -2407/-2405 and 4441/4443, numbered according to the LETO gene sequence, one of which was lost. The promoter region, the first and second exons were missing in the mutant. The region upstream and downstream of the deletion, including exons 3, 4 and 5, was conserved between the two strains, and did not contain any base changes. We found that the gene mapped to chromosome 14 in rats. OLETF rats are the naturally occurring knockout animals with the homozygously disrupted CCKAR gene. (C) 1997 Elsevier Science B.V.