Insulin Receptor anticorps (N-Term)

N° du produit ABIN392002

Cet anticorps Lapin Polyclonal détecte spécifiquement Insulin Receptor dans WB et IHC (p). Il présente une réactivité envers Souris.

Aperçu rapide pour Insulin Receptor anticorps (N-Term) (ABIN392002)

Antigène: Insulin Receptor (INSR)

Reactivité: Souris

Hôte: Lapin

Clonalité: Polyclonal

Conjugué: Cet anticorp Insulin Receptor est non-conjugé

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

Clone: RB01419

Détail du produit anti-Insulin Receptor anticorps

Épitope: AA 28-57, N-Term

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

Immunogène: 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

Information d'application

Indications d'application: WB: 1:1000. IHC-P-Leica: 1:500

Restrictions: For Research Use only

Stockage

Format: Liquid

Buffer: Purified polyclonal antibody supplied in 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.

Stock: 4 °C,-20 °C

Stockage commentaire: 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.

Date de péremption: 6 months

Détails sur Insulin Receptor

Antigène: Insulin Receptor (INSR)

Autre désignation: INSR (Insulin Receptor)

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.

Poids moléculaire: 156333

ID gène: 3643

NCBI Accession: NP_000199, NP_001073285

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