Insulin Receptor antibody (N-Term)

Catalog No. ABIN392002

This Rabbit Polyclonal antibody specifically detects Insulin Receptor in WB and IHC (p). It exhibits reactivity toward Mouse.

Quick Overview for Insulin Receptor antibody (N-Term) (ABIN392002)

Target: Insulin Receptor (INSR)

Reactivity: Mouse

Host: Rabbit

Clonality: Polyclonal

Conjugate: This Insulin Receptor antibody is un-conjugated

Application: Western Blotting (WB), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))

Clone: RB01419

Product Details anti-Insulin Receptor Antibody

Binding Specificity: AA 28-57, N-Term

Purification: This antibody is purified through a protein A column, followed by peptide affinity purification.

Immunogen: This INSR(Insulin Receptor) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 28-57 amino acids from the N-terminal region of human INSR(Insulin Receptor).

Isotype: IgG

Application Details

Application Notes: WB: 1:1000. IHC-P-Leica: 1:500

Restrictions: For Research Use only

Handling

Format: Liquid

Buffer: Purified polyclonal antibody supplied in PBS with 0.09 % (W/V) sodium azide.

Preservative: Sodium azide

Precaution of Use: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Storage: 4 °C,-20 °C

Storage Comment: Maintain refrigerated at 2-8 °C for up to 6 months. For long term storage store at -20 °C in small aliquots to prevent freeze-thaw cycles.

Expiry Date: 6 months

Target Details for Insulin Receptor

Target: Insulin Receptor (INSR)

Alternative Name: INSR (Insulin Receptor)

Background: INSR is a receptor that binds insulin and has a tyrosine-protein kinase activity. Autophosphorylation activates the kinase activity. This Type I mebrane protein is composed of a tetramer of 2 alpha and 2 beta chains linked by disulfide bonds. The alpha chains contribute to the formation of the ligand-binding domain, while the beta chains carry the kinase domain. After being transported from the endoplasmic reticulum to the Golgi apparatus, the single glycosylated precursor is further glycosylated and then cleaved, followed by its transport to the plasma membrane. Defects in INSR are the cause of insulin resistance of various forms, including mild insulin-resistant diabetes mellitus with acanthosis nigricans, minor physical abnormalities and sometimes polycystic ovaries. Insulin resistance associated with acanthosis nigricans, hirsutism and hyperandrogenism is referred to as insulin resistance type A. Defects in INSR are the cause of Rabson-Mendenhall syndrome, also known as Mendenhall syndrome. It is a severe insulin resistance syndrome characterized by insulin-resistant diabetes mellitus with pineal hyperplasia and somatic abnormalities. Typical features include coarse, senile-appearing facies, dental and skin abnormalities, abdominal distension, and phallic enlargement. Inheritance is autosomal recessive. Defects in INSR are the cause of leprechaunism, also known as Donohue syndrome. Leprechaunism represents the most severe form of insulin resistance syndrome, characterized by intrauterine and postnatal growth retardation and death in early infancy. Inheritance is autosomal recessive. Defects in INSR may be associated with noninsulin-dependent diabetes mellitus.

Molecular Weight: 156333

Gene ID: 3643

NCBI Accession: NP_000199, NP_001073285

UniProt: P06213

Pathways: NF-kappaB Signaling, RTK Signaling, AMPK Signaling, Carbohydrate Homeostasis, Regulation of Cell Size, Regulation of Carbohydrate Metabolic Process, Growth Factor Binding, Negative Regulation of Transporter Activity