Key features and details
- Goat polyclonal to PDX1
- Reacts with: Mouse, Human
- Isotype: IgG
- Research with confidence – consistent and reproducible results with every batch
- Long-term and scalable supply – powered by recombinant technology for fast production
- Success from the first experiment – confirmed specificity through extensive validation
- Ethical standards compliant – production is animal-free
Product nameAnti-PDX1 antibody
See all PDX1 primary antibodies
DescriptionGoat polyclonal to PDX1
Species reactivityReacts with: Mouse, Human
Recombinant fusion protein containing sequence from the N-terminus of mouse PDX1
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
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FunctionActivates insulin, somatostatin, glucokinase, islet amyloid polypeptide and glucose transporter type 2 gene transcription. Particularly involved in glucose-dependent regulation of insulin gene transcription. Binds preferentially the DNA motif 5'-[CT]TAAT[TG]-3'. During development, specifies the early pancreatic epithelium, permitting its proliferation, branching and subsequent differentiation. At adult stage, required for maintaining the hormone-producing phenotype of the beta-cell.
Tissue specificityDuodenum and pancreas (Langerhans islet beta cells and small subsets of endocrine non-beta-cells, at low levels in acinar cells).
Involvement in diseaseDefects in PDX1 are a cause of pancreatic agenesis (PAC) [MIM:260370]. This autosomal recessive disorder is characterized by absence or hypoplasia of pancreas, leading to early-onset insulin-dependent diabetes mellitus. This was found in a frameshift mutation that produces a truncated protein and results in a second initiation that produces a second protein that act as a dominant negative mutant.
Defects in PDX1 are a cause of non-insulin-dependent diabetes mellitus (NIDDM) [MIM:125853]; also known as diabetes mellitus type 2. NIDDM is characterized by an autosomal dominant mode of inheritance, onset during adulthood and insulin resistance.
Defects in PDX1 are the cause of maturity-onset diabetes of the young type 4 (MODY4) [MIM:606392]; also symbolized MODY-4. MODY 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 similaritiesBelongs to the Antp homeobox family. IPF1/XlHbox-8 subfamily.
Contains 1 homeobox DNA-binding domain.
DomainThe Antp-type hexapeptide mediates heterodimerization with PBX on a regulatory element of the somatostatin promoter.
The homeodomain, which contains the nuclear localization signal, not only mediates DNA-binding, but also acts as a protein-protein interaction domain for TCF3(E47), NEUROD1 and HMG-I(Y).
modificationsPhosphorylated by the SAPK2 pathway at high intracellular glucose concentration.
- Information by UniProt
- Glucose sensitive factor antibody
- Glucose-sensitive factor antibody
- GSF antibody
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
ab47383 has been referenced in 42 publications.
- Yu XX et al. Defining multistep cell fate decision pathways during pancreatic development at single-cell resolution. EMBO J 38:N/A (2019). PubMed: 30737258
- Shi Y et al. Targeting LIF-mediated paracrine interaction for pancreatic cancer therapy and monitoring. Nature 569:131-135 (2019). PubMed: 30996350
- Spaeth JM et al. The Pdx1-Bound Swi/Snf Chromatin Remodeling Complex Regulates Pancreatic Progenitor Cell Proliferation and Mature Islet ß-Cell Function. Diabetes 68:1806-1818 (2019). PubMed: 31201281
- Villani V et al. SOX9+/PTF1A+ Cells Define the Tip Progenitor Cells of the Human Fetal Pancreas of the Second Trimester. Stem Cells Transl Med 8:1249-1264 (2019). PubMed: 31631582
- Yang L et al. EGF suppresses the expression of miR-124a in pancreatic ß cell lines via ETS2 activation through the MEK and PI3K signaling pathways. Int J Biol Sci 15:2561-2575 (2019). PubMed: 31754329
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