Insulin Antikörper (N-Term)

Produktnummer ABIN5530710

Produktdetails anti-Insulin Antikörper

Target: Insulin (INS)

Bindungsspezifität: AA 21-52, N-Term

Reaktivität: Human, Maus

Wirt: Kaninchen

Klonalität: Polyklonal

Konjugat: Dieser Insulin Antikörper ist unkonjugiert

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

Aufreinigung: 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 21-52 amino acids from the N-terminal region of human INSR(Insulin Receptor).

Isotyp: Ig Fraction

Anwendungsinformationen

Applikationshinweise: For WB starting dilution is: 1:2000

For IHC-P starting dilution is: 1:50~100

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Liquid

Konzentration: 0.42 mg/mL

Buffer: Supplied in 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.

Lagerung: 4 °C,-20 °C

Informationen zur Lagerung: Store at 4°C for three months and -20°C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

Details zu Insulin

Target: Insulin (INS)

Andere Bezeichnung: INS (INS Produkte)

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.

Molekulargewicht: 156 kDa

Gen-ID: 3643

UniProt: P06213

Pathways: NF-kappaB Signalweg, RTK Signalweg, Positive Regulation of Peptide Hormone Secretion, Peptide Hormone Metabolism, Hormone Activity, Carbohydrate Homeostasis, ER-Nucleus Signaling, Regulation of Carbohydrate Metabolic Process, Feeding Behaviour, Autophagie, Negative Regulation of intrinsic apoptotic Signaling, Brown Fat Cell Differentiation, Positive Regulation of fat Cell Differentiation