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Validated All-in-One™ qPCR Primer for PDX1(NM_000209.3) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
The protein encoded by this gene is a transcriptional activator of several genes, including insulin, somatostatin, glucokinase, islet amyloid polypeptide, and glucose transporter type 2. The encoded nuclear protein is involved in the early development of the pancreas and plays a major role in glucose-dependent regulation of insulin gene expression. Defects in this gene are a cause of pancreatic agenesis, which can lead to early-onset insulin-dependent diabetes mellitus (NIDDM), as well as maturity onset diabetes of the young type 4 (MODY4). [provided by RefSeq].
Gene References into function
- differentiation factor during embryogenesis and a regulator of islet cell physiology in mature islet cells
- Conserved sequences in a tissue-specific regulatory region of the pdx-1 gene mediate transcription in Pancreatic beta cells
- differentiation of a human pancreatic duct cell line into endocrine cells: involvement of PDX-1 and HNF3beta transcription factors
- Cell-specific expression of the glucagon gene can only occur when Pdx1 expression extinguishes from the early alpha cell precursor.
- Re-expression of PDX-1 may represent a return to a more de-differentiated state by more aggressive pancreatic cancers
- insulin promoter factor 1 level is critical for human pancreas formation
- Analysis of the regulatory region of the LRH-1 gene demonstrated the presence of three functional binding sites for PDX1.
- PDX-1 represents a candidate switch factor for glandular exocrine and endocrine transdifferentiation in chronic gastritis and that an impaired parietal cell differentiation might play a key role in disturbed gastric morphogenic processes.
- E224K showed reduced transactivation activity. IPF1 mutations leading to synthesis of mutant protein may contribute to development of familial early-onset diabetes/maturity-onset diabetes of young in Indo-Trinidadians.
- PDX-1 is activated at a specific binding site in the human insulin gene
- the effect of pdx-1 expression during in vitro differentiation of embryonic stem cells
- Stable overexpression of pancreatic duodenal homeobox-1 results in repression of the endogenous human lactase-phlorizin hydrolase gene in differentiated Caco-2 cells
- Polymorphism D76N does not confer sussceptibility to type 2 diabettes.
- Hepatic regeneration and enforced PDX-1 expression accelerate transdifferentiation in liver.
- co-expression and functional synergism of these beta-cell enriched transactivators, MafA, Pdx1, and Beta2, are critical for establishing the beta-cell-specific and efficient expression of the insulin gene.
- the P33T IPF1 mutation may provide an increased susceptibility to the development of gestational diabetes and MODY4 in the Italy-6 pedigree
- Pdx-1 plays a novel role in linking H3-Lys-4 dimethylation and pol II elongation to insulin transcription
- The common alleles of regulatory variants in the 5' enhancer and promoter regions of the IPF1 gene increase susceptibility to type 2 diabetes among African American individuals.
- Analysis of both exons of the Ipf-1 coding sequence from the presented patient's genomic DNA did not identify a mutation.
- PDX-1 proteins are rapidly internalized by lipid raft-dependent macropinocytosis in HeLa cells.
- IPF1/PDX1 protein can be phosphorylated in vivo in pancreatic beta-cells; this phosphorylation marks the protein for degradation by the proteasome machinery.
- The overexpression of Pdx1 enhanced expression of pancreatic enriched genes, induction of insulin expression may require additional signals that are only present in vivo.
- Mutations in a pedigree reveals in a point mutation, increasing susceptibility to type 2 diabetes.
- The putative pancreatic stem cells expressed pdx-1 and nestin.
- pancreatic duodenal homeobox (PDX)-1 expression decreased with age in pancreatic tissue sections of humans. data provide a possible explanation for the increased incidence of type 2 diabetes at an older age
- InsCCG243 does not act in a dominant, highly penetrant fashion in African Americans and is not a significant risk factor for type 2 diabetes in this population.
- Interaction of endogenous PDX-1 and PCIF1 in MIN6 insulinoma cells, is demonstarted.
- Ex vivo lentiviral-mediated PDX1 expression in isolated adult liver cells represents a potential model for type 1 diabetes mellitus therapy.
- Human bone marrow-derived mesenchymal stem cells (hMSCs) could be induced to differentiate into functional insulin-producing cells by introduction of the pancreatic duodenal homeobox-1 (PDX-1).
- A study evaluating the extent to which common variation in the six known maturity-onset diabetes of the young (MODY) genes, which cause a monogenic form of type 2 diabetes, is associated with type 2 diabetes is presented.
- possible relationship between PDX-1 and the state of islet proliferation, islet-to-ductal transdifferentiation, apoptosis, and the expression of SSTRs
- D76N IPF1 is not contributing to type 2 diabete in early-onset or late-onset cohorts in the currently present worldwide dataset (Meta-analysis)
- This study suggests a dual role for PDX-1 in liver: inducing hepatic dedifferentiation and activating the pancreatic lineage.
- Activin B is a potent inducer of Pdx1 as well as Shh in differentiating embryonic stem cell derived embryoid bodies
- The up-regulation of PDX-1 may be an important mechanism in the induction of the Ulcer-associated cell lineage in Crohn's disease.
- The addition of betacellulin and nicotinamide sustained PDX1 expression and induced beta-cell differentiation. C-peptide-a genuine marker of de novo insulin production-was identified in the differentiated cells.
- Anomalous migration of Pdx-1 on SDS-PAGE does not result from post-translational modifications.
- PDX1 expression is lost in gastric cancers. Its effect on cell proliferation/apoptosis, migration and tumor formation in vitro and in vivo suggested that this protein functions as a putative tumor suppressor in gastric cancer.
- Under diabetic conditions, expression and/or activities of PDX-1 and MafA in beta-cells are reduced [REVIEW].
- Significance of large Maf proteins to Pdx1 expression in beta cells, and in particular MafB during pancreatic development.
- concomitant expression of Pax6 and Pdx1 is important for glucose-dependent insulinotropic polypeptide expression
- PDX-1 regulates cell proliferation and invasion in pancreatic cancer cells. Down-regulation of PDX-1 expression inhibits pancreatic cancer cell growth in vitro and in vivo.
- PDX1 is exclusively expressed in the cytoplasmic compartment in solid pseudopapillary tumours.
- PPARgamma regulates pdx-1 transcription in beta-cells
- PDX-1 expression did not correlate with biochemical recurrence of prostate cancer, but decreased with higher Gleason pattern (p<0.001) and in metastases vs primary prostate cancer (p<0.001).
- Recapitulation of pancreatic neuroendocrine tumors in human multiple endocrine neoplasia type I syndrome via Pdx1-directed inactivation of Men1.
