Insulin antibody (N-Term)

Catalog No. ABIN5530710

The Rabbit Polyclonal anti-Insulin antibody has been validated for WB and IHC (p). It is suitable to detect Insulin in samples from Human and Mouse.

Quick Overview for Insulin antibody (N-Term) (ABIN5530710)

Target: Insulin (INS)

Reactivity: Human, Mouse

Host: Rabbit

Clonality: Polyclonal

Conjugate: This Insulin antibody is un-conjugated

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

Product Details anti-Insulin Antibody

Binding Specificity: AA 21-52, 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 21-52 amino acids from the N-terminal region of human INSR(Insulin Receptor).

Isotype: Ig Fraction

Application Details

Application Notes: For WB starting dilution is: 1:2000

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

Restrictions: For Research Use only

Handling

Format: Liquid

Concentration: 0.42 mg/mL

Buffer: 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: 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.

Target Details for Insulin

Target: Insulin (INS)

Alternative Name: INS

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: 156 kDa

Gene ID: 3643

UniProt: P06213

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