CALM2 Antibody | 23-348

CALM2 Antibody | 23-348 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse, Rat

Homology: N/A

Immunogen: Recombinant fusion protein containing a sequence corresponding to amino acids 1-149 of human CALM2 (NP_001734.1) .

Research Area: Cell Cycle, Immunology, Neuroscience, Signal Transduction

Tested Application: WB

Application: WB: 1:500 - 1:2000

Specificiy: N/A

Positive Control 1: NIH/3T3

Positive Control 2: MCF7

Positive Control 3: BT-474

Positive Control 4: NCI-H460

Positive Control 5: Mouse brain

Positive Control 6: N/A

Molecular Weight: Observed: 17kDa

Validation: N/A

Isoform: N/A

Purification: Affinity purification

Clonality: Polyclonal

Clone: N/A

Isotype: IgG

Conjugate: Unconjugated

Physical State: Liquid

Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.

Concentration: N/A

Storage Condition: Store at -20˚C. Avoid freeze / thaw cycles.

Alternate Name: CALM, CAM, CAM1, CALM2, CAM2, CAMB, CALM3, CALML2, CAM3, CAMC, CAMIII, CalmodulinCaM, caM, CAMI, PHKD, CPVT4, DD132

User Note: Optimal dilutions for each application to be determined by the researcher.

BACKGROUND: This gene is a member of the calmodulin gene family. There are three distinct calmodulin genes dispersed throughout the genome that encode the identical protein, but differ at the nucleotide level. Calmodulin is a calcium binding protein that plays a role in signaling pathways, cell cycle progression and proliferation. Several infants with severe forms of long-QT syndrome (LQTS) who displayed life-threatening ventricular arrhythmias together with delayed neurodevelopment and epilepsy were found to have mutations in either this gene or another member of the calmodulin gene family (PMID:23388215) . Mutations in this gene have also been identified in patients with less severe forms of LQTS (PMID:24917665) , while mutations in another calmodulin gene family member have been associated with catecholaminergic polymorphic ventricular tachycardia (CPVT) (PMID:23040497) , a rare disorder thought to be the cause of a significant fraction of sudden cardiac deaths in young individuals. Pseudogenes of this gene are found on chromosomes 10, 13, and 17. Alternative splicing results in multiple transcript variants encoding different isoforms.