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Product Description
CISD2 Antibody | 7301 | ProSci
Host: Rabbit
Reactivity: Human, Mouse, Rat
Homology: Predicted species reactivity based on immunogen sequence: Bovine: (100%)
Immunogen: CISD2 antibody was raised against a 15 amino acid peptide near the center of human CISD2.
The immunogen is located within amino acids 40 - 90 of CISD2.
Research Area: Autophagy
Tested Application: E, WB, IHC-P, IF
Application: CISD2 antibody was raised against a 15 amino acid peptide near the center of human CISD2.
Antibody validated: Western Blot in rat samples; Immunohistochemistry in rat samples and Immunofluorescence in rat samples. All other applications and species not yet tested.
Specificiy: N/A
Positive Control 1: Cat. No. 1463 - Rat Brain Tissue Lysate
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: Predicted: 15 kDa
Observed: 15 kDa
Validation: N/A
Isoform: N/A
Purification: CISD2 Antibody is affinity chromatography purified via peptide column.
Clonality: Polyclonal
Clone: N/A
Isotype: IgG
Conjugate: Unconjugated
Physical State: Liquid
Buffer: CISD2 Antibody is supplied in PBS containing 0.02% sodium azide.
Concentration: 1 mg/mL
Storage Condition: CISD2 antibody can be stored at 4˚C for three months and -20˚C, stable for up to one year.
Alternate Name: CISD2 Antibody: ERIS, WFS2, ZCD2, NAF-1, Miner1, CDGSH2, ERIS, CDGSH iron-sulfur domain-containing protein 2, Endoplasmic reticulum intermembrane small protein
User Note: Optimal dilutions for each application to be determined by the researcher.
BACKGROUND: CISD2 Antibody: Defects in the CISD2 (CDGSH iron sulfur domain 2) gene are a cause of the neurodegenerative disorder Wolfram syndrome 2. CISD2 is a zinc finger protein that localizes to the endoplasmic reticulum and mitochondria and binds an iron/sulfur cluster. CISD2 interacts with Bcl-2 and can be displaced by the BH3-only protein BIK and contributes to the regulation of BIK-initiated autophagy. CISD2 deficiency in mice causes mitochondrial breakdown accompanied by autophagic cell death as well as the development of premature aging phenotype.
