Insulin Receptor Antikörper (N-Term)

Produktnummer ABIN359886

Der Kaninchen Polyklonal anti-Insulin Receptor Antikörper (ABIN359886) detektiert spezifisch Insulin Receptor in WB, IHC (p) und EIA. Dieser Antikörper reagiert spezifisch mit Proben aus Human.

Kurzübersicht für Insulin Receptor Antikörper (N-Term) (ABIN359886)

Target: Insulin Receptor (INSR)

Reaktivität: Human

Wirt: Kaninchen

Klonalität: Polyklonal

Konjugat: Dieser Insulin Receptor Antikörper ist unkonjugiert

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

Produktdetails anti-Insulin Receptor Antikörper

Bindungsspezifität: N-Term

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

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

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

Isotyp: Ig Fraction

Anwendungsinformationen

Applikationshinweise: ELISA: 1/1,000. Western blotting: 1/100 - 1/500. Immunohistochemistry: 1/50 - 1/100.

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Liquid

Konzentration: 0.25 mg/mL

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

Konservierungsmittel: Sodium azide

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

Handhabung: Avoid repeated freezing and thawing.

Lagerung: 4 °C/-20 °C

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

Details zu Insulin Receptor

Target: Insulin Receptor (INSR)

Andere Bezeichnung: CD220 / INSR

Hintergrund: 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

Gen-ID: 3643, 9606

UniProt: P06213

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