The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use at an assay dependent concentration. PubMed: 24336520
Use at an assay dependent concentration. PubMed: 20335226
1/50 - 1/100.
1/50 - 1/100. Prolonged fixation in buffered formalin can destroy the epitope.
1/50 - 1/100.
Use at an assay dependent concentration. PubMed: 21829502
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.
Immunohistochemistry (Frozen sections) - Anti-Insulin antibody (ab7842)This image is courtesy of an anonymous Abreview.
ab7842 staining Insulin in human kidney tissue by Immunohistochemistry (Frozen sections). Tissue was fixed in formaldehyde, permeabilized with methanol , blocked using 3% BSA for 1 hour at 22°C then incubated with ab7842 at a 1/200 dilution for 18 hours at 4°C. The secondary used was an Aleza-Fluor 568 conjugated goat anti-guinea pig polyclonal used at a 1/500 dilution. Image shows kidney section bearing RGD-Adv-hHGF-hXIAP-transduced human islets at 30 days after islet transplantation. (a-b) Insulin was stained in red to indicate the functional human islets of mice receiving untransduced human islets (a) and RGD-Adv-hHGF-hXIAP-transduced human islets (b).
This image was kindly supplied as part of the review submitted by Kristi Hultman.
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Insulin antibody (ab7842)This image is courtesy of an Abreview submitted by Dr Ulrich Schweizer
ab7842 at 1/1000 dilution staining rat pancreas tissue sections by Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections). The sections were fixed with paraformaldehyde and blocked with 5% serum prior to incubation with the antibody for 12 hours. A Cy2 conjuagted goat polyclonal antibody was used as the secondary. Insulin staining is shown in green. Somatostatin staining is shown in red. DAPI was used as nuclear counterstain.
Lines KE et al. Epigenetic pathway inhibitors represent potential drugs for treating pancreatic and bronchial neuroendocrine tumors. Oncogenesis6:e332 (2017).
Read more (PubMed: 28504695) »
Perez-Basterrechea M et al. Fibroblasts accelerate islet revascularization and improve long-term graft survival in a mouse model of subcutaneous islet transplantation. PLoS One12:e0180695 (2017).
Read more (PubMed: 28672010) »