Overview

  • Product name

  • Description

    Rabbit polyclonal to Insulin
  • Host species

    Rabbit
  • Tested applications

    Suitable for: IHC-Pmore details
  • Species reactivity

    Reacts with: Mouse, Rat
    Predicted to work with: Human
  • Immunogen

    Synthetic peptide within Human Insulin aa 45-95 conjugated to keyhole limpet haemocyanin. The exact sequence is proprietary.
    Sequence:

    ERGFFYTPKTRREAEDLQVGQVELGGGPGAGSLQPLALEGSLQKRGIVEQ C


    Database link: P01308

  • Positive control

    • Mouse and Rat pancreas tissue.

Properties

Applications

Our Abpromise guarantee covers the use of ab216418 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
IHC-P 1/100 - 1/500.

When using a fluorescent secondary probe the recommended dilution is 1/50 - 1/200.

Target

  • Function

    Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.
  • Involvement in disease

    Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:176730].
    Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:125852]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.
    Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:606176]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.
    Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:613370]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.
  • Sequence similarities

    Belongs to the insulin family.
  • Cellular localization

    Secreted.
  • Information by UniProt
  • Database links

  • Alternative names

    • IDDM antibody
    • IDDM1 antibody
    • IDDM2 antibody
    • ILPR antibody
    • ins antibody
    • INS_HUMAN antibody
    • Insulin A chain antibody
    • Insulin B chain antibody
    • IRDN antibody
    • MODY10 antibody
    • Preproinsulin antibody
    • Proinsulin antibody
    • Proinsulin precursor antibody
    see all

Images

  • Immunohistochemical analysis of formalin-fixed, paraffin-embedded Mouse pancreas labeling Insulin with ab216418 at 1/200 dilution followed by conjugation to the secondary antibody and DAB staining.

  • Immunohistochemical analysis of formalin-fixed, paraffin-embedded Rat pancreas tissue labeling Insulin with ab216418 at 1/200 dilution followed by Goat anti-rabbit IgG, FITC conjugated, at 1/200 dilution for 40 minutes at 37°C.

References

ab216418 has not yet been referenced specifically in any publications.

Customer reviews and Q&As

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