Insulin Receptor anticorps (N-Term)

N° du produit ABIN359886

Cet anticorps anti-Insulin Receptor Polyclonal Lapin (ABIN359886) détecte spécifiquement Insulin Receptor dans WB, IHC (p) et EIA. L’anticorps est réactif avec des échantillons de Humain.

Aperçu rapide pour Insulin Receptor anticorps (N-Term) (ABIN359886)

Antigène: Insulin Receptor (INSR)

Reactivité: Humain

Hôte: Lapin

Clonalité: Polyclonal

Conjugué: Cet anticorp Insulin Receptor est non-conjugé

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

Détail du produit anti-Insulin Receptor anticorps

Épitope: N-Term

Specificité: This antibody reacts to INSR (Insulin Receptor).

Purification: Protein G column, eluted with high and low pH buffers and neutralized immediately, followed by dialysis against PBS

Immunogène: This antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide selected from the N-terminal region of human INSR.

Isotype: Ig Fraction

Information d'application

Indications d'application: ELISA: 1/1,000. Western blotting: 1/100 - 1/500. Immunohistochemistry: 1/50 - 1/100.

Restrictions: For Research Use only

Stockage

Format: Liquid

Concentration: 0.25 mg/mL

Buffer: PBS with 0.09 % (W/V) sodium azide

Agent conservateur: Sodium azide

Précaution d'utilisation: This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Conseil sur la manipulation: Avoid repeated freezing and thawing.

Stock: 4 °C/-20 °C

Stockage commentaire: Store the antibody undiluted at 2-8 °C for one month or (in aliquots) at-20 °C for longer.

Détails sur Insulin Receptor

Antigène: Insulin Receptor (INSR)

Autre désignation: CD220 / INSR

Sujet: 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.Synonyms: Insulin Receptor

ID gène: 3643, 9606

UniProt: P06213

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