HMG-CoA reductase is the rate-limiting enzyme for cholesterol synthesis and is regulated via a negative feedback mechanism mediated by sterols and non-sterol metabolites derived from mevalonate, the product of the reaction catalyzed by reductase. Normally in mammalian cells this enzyme is suppressed by cholesterol derived from the internalization and degradation of low density lipoprotein (LDL) via the LDL receptor. Competitive inhibitors of the reductase induce the expression of LDL receptors in the liver, which in turn increases the catabolism of plasma LDL and lowers the plasma concentration of cholesterol, an important determinant of atherosclerosis. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.

Pack Size

100ul, 1ml, 20ul

Applications

ELISA, WB

Host Species

Rabbit

Ig Isotype

IgG

Antibody Type

Monoclonal Antibody

Organism Species

Human

Concentration

Product Synonyms

HMGCR

Observed Mol Wt

97kDa

Alternative Names

LDLCQ3; HMGCR

Immunogen (Antigen)

synthetic peptide

Format

Liquid

Buffer Formulation

0.05% BSA, 50% glycerol, PBS with 0.02% sodium azide, pH7.3

Reactivity

Human, Mouse, Rat

Uniprot ID

3156

Gene ID

P04035

Potency (Clone Number)

ARC0496

Purification

Antigen-specific affinity chromatography followed by Protein A affinity chromatography

Usage

For Research Use Only. Not for diagnostics or human use.

Shelf Life

12 months at time of shipping

Shipping

Shipped in Dry Ice at -20 Degree Celsius

Storage

Store at -20 Degree Celsius. It is recommended to aliquot and store to avoid repeated freeze-thaw as it affects the stability of the antibody.

Research Areas

Cancer, Cell Biology, Immunology

KD/KO Validated

KD Validated

Disclaimer

The data indicated herein are as indicated and validated in our laboratory. These reagents are for research use only and not for in-vitro diagnostics or human use.

Reviews

There are no reviews yet.

Be the first to review “HMGCR Rabbit Monoclonal Antibody”

Your email address will not be published. Required fields are marked *