Human CALHM1 blocking peptide (CDBP0661)

Synthetic Human CALHM1 blocking peptide for BL

Product Overview
Blocking peptide for anti-CALHM1 antibody
Species Reactivity
Application Notes
For in vitro research use only. Not intended for any diagnostic or therapeutic purpose. Not suitable for human or animal consumption.
200 μg/ml
50 μg
PBS containing 0.02% sodium azide
0.02% Sodium Azide
Store at -20℃, stable for one year.
UniProt ID
Antigen Description
This gene encodes a calcium channel that plays a role in processing of amyloid-beta precursor protein. A polymorphism at this locus has been reported to be associated with susceptibility to late-onset Alzheimer's disease in some populations, but the pathogenicity of this polymorphism is unclear.
calcium channel activity; identical protein binding; ion channel activity;
CALHM1; calcium homeostasis modulator 1; FAM26C, family with sequence similarity 26, member C; calcium homeostasis modulator protein 1; family with sequence similarity 26, member C; FAM26C; MGC39514; MGC39617;


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No association between CALHM1 polymorphism and Alzheimer's disease risk in a Hungarian population


Authors: Feher, Agnes; Juhasz, Anna; Rimanoczy, Agnes; Pakaski, Magdolna; Kalman, Janos; Janka, Zoltan

Calcium homeostasis modulator 1 (CALHM1), a promising candidate gene for Alzheimer's disease risk, has been recently identified. We tested the hypothesis that the T-allelic variant of the CALHM1 rs2986017 polymorphism confers susceptibility to Alzheimer's disease in a Hungarian case-control sample that was also genotyped for apolipoprotein E. This study included 238 probable patients with Alzheimer's disease who met the diagnostic criteria for National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association and 202 elderly healthy control participants. We failed to detect an association between the CALHM1 polymorphism and the risk for Alzheimer's disease (P = 0.153 for genotypes and P = 0.090 for alleles), nor did we find an effect on age at onset. However, a potential weak correlation between the presence of the T allele (CT and TT genotypes together) and Alzheimer's disease was observed (P = 0.056). Psychiatr Genet 21:249-252 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.

Greater reductions in fat preferences in CALHM1 than CD36 knockout mice


Authors: Sclafani, Anthony; Ackroff, Karen

Several studies indicate an important role of gustation in intake and preference for dietary fat. The present study compared fat preference deficits produced by deletion of CD36, a putative fatty acid taste receptor, and CALHM1, an ion channel responsible for release of the ATP neurotransmitter used by taste cells. Naive CD36 knockout (KO) mice displayed reduced preferences for soybean oil emulsions (Intralipid) at low concentrations (0.1-1%) compared with wild-type (WT) mice in 24 h/day two-bottle tests. CALHM1 KO mice displayed even greater Intralipid preference deficits compared with WT and CD36 KO mice. These findings indicate that there may be another taste receptor besides CD36 that contributes to fat detection and preference. After experience with concentrated fat (2.5-5%), CD36 KO and CALHM1 KO mice displayed normal preferences for 0.1-5% fat, although they still consumed less fat than WT mice. The experience-induced rescue of fat preferences in KO mice can be attributed to postoral fat conditioning. Short-term (3-min) two-bottle tests further documented the fat preference deficits in CALHM1 KO mice but also revealed residual preferences for concentrated fat (5-10%), which may be mediated by odor and/or texture cues.

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