MECR Antibody | 7151

MECR Antibody | 7151 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse, Rat

Homology: Predicted species reactivity based on immunogen sequence: Bovine: (100%)

Immunogen: Rabbit polyclonal MECR antibody was raised against a 15 amino acid peptide near the carboxy terminus of human MECR.
The immunogen is located within amino acids 300 - 350 of MECR.

Research Area: Homeostasis

Tested Application: E, WB

Application: MECR antibody can be used for detection of MECR by Western blot at 1 - 2 μg/mL.
Antibody validated: Western Blot in human, mouse, and rat samples. All other applications and species not yet tested.

Specificiy: At least two isoforms of MECR are known to exist; this antibody will detect both isoforms.

Positive Control 1: Cat. No. 1303 - Human Brain Tissue Lysate

Positive Control 2: Cat. No. 1403 - Mouse Brain Tissue Lysate

Positive Control 3: Cat. No. 1463 - Rat Brain Tissue Lysate

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: Predicted: 41 kDa

Validation: N/A

Isoform: N/A

Purification: MECR Antibody is affinity chromatography purified via peptide column.

Clonality: Polyclonal

Clone: N/A

Isotype: IgG

Conjugate: Unconjugated

Physical State: Liquid

Buffer: MECR Antibody is supplied in PBS containing 0.02% sodium azide.

Concentration: 1 mg/mL

Storage Condition: MECR antibody can be stored at 4˚C for three months and -20˚C, stable for up to one year.

Alternate Name: MECR Antibody: NRBF1, CGI-63, FASN2B, NBRF1, Trans-2-enoyl-CoA reductase, mitochondrial, Nuclear receptor-binding factor 1, HsNrbf-1

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

BACKGROUND: MECR Antibody: The mitochondrial trans-2-enoyl-CoA reductase (MECR) , was initially identified as nuclear receptor-binding factor 1 (NRBF1) , which can interact with a multitude of nuclear hormone receptors in the presence of the respective ligands. MECR has been shown to be part of the mitochondrial fatty acid synthesis (FAS II) system and to catalyze the NAPDH-dependent reduction of 2-enoyl thioesters, generating saturated acyl-groups. Overexpression of this gene in transgenic mice can lead to cardiac abnormalities, suggesting that inappropriate expression of genes of FAS II can result in the development of hereditary cardiomyopathy.