LDLR mouse monoclonal antibody,clone OTI1F4

Name: LDLR mouse monoclonal antibody,clone OTI1F4
SKU: GAM923620
Price: 169 CNY
Availability: InStock

AliasesLDL Receptor

ReactivityHuman

ApplicationsFC

Host / ClonalityMouse / Monoclonal

Lead timeIn stock · ships in 48h

$169/ 50μlIn stock 199 · Ready to ship

50μl$169

100μl$299

Applications & Recommended Dilution

Applications & DilutionRecommended Dilution

Recommended dilutionNo data

Reactivity: Human
Assay: FC

Product Images

Product ImagesImages

LDLR mouse monoclonal antibody,clone OTI1F4 图 1 — Image 1Flow cytometric analysis of living 293T cells transfected with LDLR overexpression plasmid, Red)/empty vector (Blue) using anti-LDLR antibody (GAM923620). Cells incubated with a non-specific antibody (Green) were used as isotype control (1:100).

Product Specifications

SpecificationsProduct Specifications

Core Attributes CORE ATTRIBUTES

Species Reactivity: Human

Applications: FC

Clone name: OTI1F4

Calculated molecular weight: 95.38 kDa

Immunogen: Full length human recombinant protein of human LDLR (NP_000518) produced in HEK293T cell.

Isotype: IgG1

Host species: Mouse

Clonality: Monoclonal

Purification method: Affinity Purification

Uniprot-A: P01130

Product Properties PRODUCT PROPERTIES

Shipping: They are shipped out with dry ice/blue ice unless customers require otherwise

Storage Condition: Store at -20°C PBS (pH 7.3) containing 1% BSA, 50% glycerol and 0.02% sodium azide.Stable for 12 months from date of receipt.

Formulation: Liquid

Storage Buffer: PBS (pH 7.3) containing 1% BSA, 50% glycerol and 0.02% sodium azide.

The low density lipoprotein receptor (LDLR) gene family consists of cell surface proteins involved in receptor-mediated endocytosis of specific ligands. Low density lipoprotein (LDL) is normally bound at the cell membrane and taken into the cell ending up in lysosomes where the protein is degraded and the cholesterol is made available for repression of microsomal enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, the rate-limiting step in cholesterol synthesis. At the same time, a reciprocal stimulation of cholesterol ester synthesis takes place. Mutations in this gene cause the autosomal dominant disorder, familial hypercholesterolemia. Alternate splicing results in multiple transcript variants. [provided by RefSeq, Sep 2010]