Key features and details
- Guinea pig polyclonal to PDX1
- Suitable for: ICC/IF
- Reacts with: Mouse, Human
- Isotype: IgG
Product nameAnti-PDX1 antibody
See all PDX1 primary antibodies
DescriptionGuinea pig polyclonal to PDX1
Host speciesGuinea pig
Tested applicationsSuitable for: ICC/IFmore details
Species reactivityReacts with: Mouse, Human
Recombinant fusion protein containing N-terminal sequence from 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.
Concentration information loading...
Our Abpromise guarantee covers the use of ab47308 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
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
ab47308 has been referenced in 23 publications.
- Legøy TA et al. Encapsulation boosts islet-cell signature in differentiating human induced pluripotent stem cells via integrin signalling. Sci Rep 10:414 (2020). PubMed: 31942009
- Wada Y et al. The Differences in the Characteristics of Insulin-producing Cells Using Human Adipose-tissue Derived Mesenchymal Stem Cells from Subcutaneous and Visceral Tissues. Sci Rep 9:13204 (2019). PubMed: 31519950
- Bru-Tari E et al. Pancreatic alpha-cell mass in the early-onset and advanced stage of a mouse model of experimental autoimmune diabetes. Sci Rep 9:9515 (2019). PubMed: 31266981
- Vethe H et al. The Effect of Wnt Pathway Modulators on Human iPSC-Derived Pancreatic Beta Cell Maturation. Front Endocrinol (Lausanne) 10:293 (2019). PubMed: 31139151
- Ng NHJ et al. HNF4A Haploinsufficiency in MODY1 Abrogates Liver and Pancreas Differentiation from Patient-Derived Induced Pluripotent Stem Cells. iScience 16:192-205 (2019). PubMed: 31195238