PAX4, Polyclonal Antibody

For Research Use Only. Not for use in diagnostic procedures.

Polyclonal

Rabbit

Small volumes of anti-PAX4 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Polyclonal

Western Blot (WB), Immunohistochemistry (IHC)

Western blot analysis of extracts of Lovo cells, using PAX4 antibody at 1:1000 dilution.
Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (MBS128200) at 1:10000 dilution.
Lysates/proteins: 25ug per lane.
Blocking buffer: 3% nonfat dry milk in TBST.
Detection: ECL Enhanced Kit.
Exposure time: 90s.

350

paired box 4

paired box protein Pax-4; paired box gene 4; paired domain gene 4

Paired box protein Pax-4

PAX4_HUMAN

This gene is a member of the paired box (PAX) family of transcription factors. Members of this gene family typically contain a paired box domain, an octapeptide, and a paired-type homeodomain. These genes play critical roles during fetal development and cancer growth. The paired box 4 gene is involved in pancreatic islet development and mouse studies have demonstrated a role for this gene in differentiation of insulin-producing beta cells. [provided by RefSeq, Jul 2008]

PAX4: Plays an important role in the differentiation and development of pancreatic islet beta cells. Transcriptional repressor that binds to a common element in the glucagon, insulin and somatostatin promoters. Competes with PAX6 for this same promoter . Isoform 2 appears to be a dominant negative form antagonizing PAX4 transcriptional activity. Defects in PAX4 are a cause of noninsulin-dependent diabetes mellitus (NIDDM); also known as diabetes mellitus type 2 or maturity-onset diabetes. NIDDM is characterized by an autosomal dominant mode of inheritance, onset during *****hood and insulin resistance. Genetic variations in PAX4 are associated with susceptibility to insulin-dependent diabetes mellitus (IDDM). IDDM normally starts in childhood or adolescence and is caused by the body's own immune system which destroys the insulin-producing beta cells in the pancreas. Classical features are polydipsia, polyphagia and polyuria, due to hyperglycemia- induced osmotic diuresis. Defects in PAX4 are a cause of susceptibility to diabetes mellitus ketosis-prone (KPD). KPD is an atypical form of diabetes mellitus characterized by an acute initial presentation with severe hyperglycemia and ketosis, as seen in classic type 1 diabetes, but after initiation of insulin therapy, prolonged remission is often possible with cessation of insulin therapy and maintenance of appropriate metabolic control. Metabolic studies show a markedly blunted insulin secretory response to glucose, partially reversible with the improvement of blood glucose control. Variable levels of insulin resistance are observed, especially in obese patients. Pancreatic beta-cell autoimmunity is a rare finding. Defects in PAX4 are the cause of maturity-onset diabetes of the young type 9 (MODY9). MODY is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early *****hood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease. Belongs to the paired homeobox family. 3 isoforms of the human protein are produced by alternative splicing.

Protein type: Transcription factor; DNA-binding

Chromosomal Location of Human Ortholog: 7q32

Cellular Component: nucleoplasm

Molecular Function: DNA binding; double-stranded DNA binding

Biological Process: response to drug; circadian rhythm; organ morphogenesis; response to cAMP; transcription, DNA-dependent; retina development in camera-type eye; negative regulation of transcription from RNA polymerase II promoter; cell differentiation; positive regulation of cell differentiation; endocrine pancreas development; negative regulation of apoptosis

Disease: Maturity-onset Diabetes Of The Young, Type 9; Diabetes Mellitus, Ketosis-prone; Diabetes Mellitus, Noninsulin-dependent

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