Search results for: Insulin promoter factor 1
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Isl1β Overexpression With Key β Cell Transcription Factors Enhances Glucose-Responsive Hepatic Insulin Production and Secretion.Adenoviral gene transfer of key β cell developmental regulators including Pdx1, Neurod1, and Mafa (PDA) has been reported to generate insulin-producing cells in the liver. However, PDA insulin secretion is transient and glucose unresponsive. Here, we report that an additional β cell developmental regulator, insulin gene enhancer binding protein splicing variant (Isl1β), improved insulin production and glucose-responsive secretion in PDA mice. Microarray gene expression analysis suggested that adenoviral PDA transfer required an additional element for mature β cell generation, such as Isl1 and Elf3 in the liver. In vitro promoter analysis indicated that splicing variant Isl1, or Isl1β, is an important factor for transcriptional activity of the insulin gene. In vivo bioluminescence monitoring using insulin promoter-luciferase transgenic mice verified that adenoviral PDA + Isl1β transfer produced highly intense luminescence from the liver, which peaked at day 7 and persisted for more than 10 days. Using insulin promoter-GFP transgenic mice, we further confirmed that Isl1β supplementation to PDA augmented insulin-producing cells in the liver, insulin production and secretion, and β cell‒related genes. Finally, the PDA + Isl1β combination ameliorated hyperglycemia in diabetic mice for 28 days and enhanced glucose tolerance and responsiveness. Thus, our results suggest that Isl1β is a key additional transcriptional factor for advancing the generation of insulin-producing cells in the liver in combination with PDA.
1597 related Products with: Isl1β Overexpression With Key β Cell Transcription Factors Enhances Glucose-Responsive Hepatic Insulin Production and Secretion.GLP 1 ELISA Kit, Rat Gluc Insulin Glucose Phospho-S Transcription Factors: N Transcription Factors: T Transcription factors: O D (+) Glucose anhydrous c Stable cell line: p53 Ov Transcription factors: N Cellufine Formyl , 50 ml Cellufine Formyl Media Cellufine Formyl , 500 ml Cellufine Amino , 50 ml
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The species origin of the cellular microenvironment influences markers of beta cell fate and function in EndoC-βH1 cells.Interaction between islet cell subtypes and the extracellular matrix influences beta-cell function in mammals. The tissue architecture of rodent islets is very different to that of human islets; cell-to-cell communication and interaction with the extracellular matrix may vary between species. In this work, we have compared the responses of the human EndoC-βH1 cell line to non-human and human-derived growth matrices in terms of growth morphology, gene expression and glucose-stimulated insulin secretion (GSIS). EndoC-βH1 cells demonstrated a greater tendency to form cell clusters when cultured in a human microenvironment and exhibited reduced alpha cell markers at the mRNA level; mean expression difference - 0.23 and - 0.51; p = 0.009 and 0.002 for the Aristaless-related homeobox (ARX) and Glucagon (GCG) genes respectively. No differences were noted in the protein expression of mature beta cell markers such as Pdx1 and NeuroD1 were noted in EndoC-βH1 cells grown in a human microenvironment but cells were however more sensitive to glucose (4.3-fold increase in insulin secretion following glucose challenge compared with a 1.9-fold increase in cells grown in a non-human microenvironment; p = 0.0003). Our data suggests that the tissue origin of the cellular microenvironment has effects on the function of EndoC-βH1 cells in vitro, and the use of a more human-like culture microenvironment may bring benefits in terms of increased physiological relevance.
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Regulation of NOTCH signaling by RAB7 and RAB8 requires carboxyl methylation by ICMT.Isoprenylcysteine carboxyl methyltransferase (ICMT) methylesterifies C-terminal prenylcysteine residues of CaaX proteins and some RAB GTPases. Deficiency of either ICMT or NOTCH1 accelerates pancreatic neoplasia in;mice, suggesting that ICMT is required for NOTCH signaling. We usedwing vein and scutellar bristle development to screen Rab proteins predicted to be substrates for ICMT (ste14 in flies). We identified Rab7 and Rab8 as ICMT substrates that when silenced phenocopy ste14 deficiency. ICMT, RAB7, and RAB8 were all required for efficient NOTCH1 signaling in mammalian cells. Overexpression of RAB8 rescued NOTCH activation afterknockdown both in U2OS cells expressing NOTCH1 and in fly wing vein development. ICMT deficiency induced mislocalization of GFP-RAB7 and GFP-RAB8 from endomembrane to cytosol, enhanced binding to RABGDI, and decreased GTP loading of RAB7 and RAB8. Deficiency of ICMT, RAB7, or RAB8 led to mislocalization and diminished processing of NOTCH1-GFP. Thus, NOTCH signaling requires ICMT in part because it requires methylated RAB7 and RAB8.
1741 related Products with: Regulation of NOTCH signaling by RAB7 and RAB8 requires carboxyl methylation by ICMT.DNA (cytosine 5) methyltr Epidermal Growth Factor ( Epidermal Growth Factor ( Androgen Receptor (Phosph Androgen Receptor (Phosph Goat Anti-Human RAB8A, C- Rabbit Anti-Human Androge Rabbit Anti-Human Androge Hh Signaling Pathway Anta Androgen Receptor (Ab 650 Acetyl CoA Carboxylase An Acetyl-CoA Carboxylase (A
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Insights From Molecular Characterization of Adult Patients of Families With Multigenerational Diabetes.Multigenerational diabetes of adulthood is a mostly overlooked entity, simplistically lumped into the large pool of type 2 diabetes. The general aim of our research in the past few years is to unravel the genetic causes of this form of diabetes. Identifying among families with multigenerational diabetes those who carry mutations in known monogenic diabetes genes is the first step to then allow us to concentrate on remaining pedigrees in which to unravel new diabetes genes. Targeted next-generation sequencing of 27 monogenic diabetes genes was carried out in 55 family probands and identified mutations verified among their relatives by Sanger sequencing. Nine variants (in eight probands) survived our filtering/prioritization strategy. After likelihood of causality assessment by established guidelines, six variants were classified as "pathogenetic/likely pathogenetic" and two as "of uncertain significance." Combining present results with our previous data on the six genes causing the most common forms of maturity-onset diabetes of the young allows us to infer that 23.6% of families with multigenerational diabetes of adulthood carry mutations in known monogenic diabetes genes. Our findings indicate that the genetic background of hyperglycemia is unrecognized in the vast majority of families with multigenerational diabetes of adulthood. These families now become the object of further research aimed at unraveling new diabetes genes.
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PDX1: A Unique Pancreatic Master Regulator Constantly Changes Its Functions during Embryonic Development and Progression of Pancreatic Cancer.Multifunctional activity of the PDX1 gene product is reviewed. The PDX1 protein is unique in that being expressed exclusively in the pancreas it exhibits various functional activities in this organ both during embryonic development and during induction and progression of pancreatic cancer. Hence, PDX1 belongs to the family of master regulators with multiple and often antagonistic functions.
1210 related Products with: PDX1: A Unique Pancreatic Master Regulator Constantly Changes Its Functions during Embryonic Development and Progression of Pancreatic Cancer.Pancreatic disease spectr Anti PDX1 Polyclonal Anti Multiple pancreatic cance Mid advanced stage pancre High density (69 cases 20 High density (69 cases 20 High density pancreatic c Pancreatic cancer test ti Multiple pancreatic cance Multiple pancreatic cance Multiple pancreatic cance Multiple pancreatic cance
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Generation of a pancreatic cancer model using a Pdx1-Flp recombinase knock-in allele.The contribution of the tumor microenvironment to the development of pancreatic adenocarcinoma (PDAC) is unclear. The LSL-KrasG12D/+;LSL-p53R172H/+;Pdx-1-Cre (KPC) tumor model, which is widely utilized to faithfully recapitulate human pancreatic cancer, depends on Cre-mediated recombination in the epithelial lineage to drive tumorigenesis. Therefore, specific Cre-loxP recombination in stromal cells cannot be applied in this model, limiting the in vivo investigation of stromal genetics in tumor initiation and progression. To address this issue, we generated a new Pdx1FlpO knock-in mouse line, which represents the first mouse model to physiologically express FlpO recombinase in pancreatic epithelial cells. This mouse specifically recombines Frt loci in pancreatic epithelial cells, including acinar, ductal, and islet cells. When combined with the Frt-STOP-Frt KrasG12D and p53Frt mouse lines, simultaneous Pdx1FlpO activation of mutant Kras and deletion of p53 results in the spectrum of pathologic changes seen in PDAC, including PanIN lesions and ductal carcinoma. Combination of this KPF mouse model with any stroma-specific Cre can be used to conditionally modify target genes of interest. This will provide an excellent in vivo tool to study the roles of genes in different cell types and multiple cell compartments within the pancreatic tumor microenvironment.
2250 related Products with: Generation of a pancreatic cancer model using a Pdx1-Flp recombinase knock-in allele.Mid advanced stage pancre Pancreatic disease spectr High density pancreatic c Pancreatic cancer tissue Multiple pancreatic cance Pancreatic cancer and nor Pancreatic cancer tissue Pancreatic cancer and nor Pancreatic cancer tissue Pancreatic cancer test ti Pancreatic cancer test ti Pancreatic cancer test ti
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Determinants of platelet count in pediatric patients with congenital cyanotic heart disease: Role of immature platelet fraction.Congenital heart defects are common noninfectious causes of mortality in children. Bleeding and thrombosis are both limiting factors in the management of such patients. We assessed the frequency of thrombocytopenia in pediatric patients with congenital cyanotic heart disease (CCHD) and evaluated determinants of platelet count including immature platelet fraction (IPF) and their role in the pathogenesis of thrombocytopenia.
2286 related Products with: Determinants of platelet count in pediatric patients with congenital cyanotic heart disease: Role of immature platelet fraction.Anti beta3 AR Human, Poly CELLKINES PLATELET DERIVE PLATELET DERIVED GROWTH F CELLKINES PLATELET DERIVE PLATELET DERIVED GROWTH F Human Platelet Derived Gr Human Platelet Derived Gr Human Platelet Derived Gr Mouse Platelet Derived Gr Mouse Platelet Derived Gr Rat platelet Selectin(P-S platelet factor 4 variant
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Dependence of expression of regulatory master genes of embryonic development in pancreatic cancer cells on the intracellular concentration of the master regulator PDX1.Exogenous expression of the gene encoding the pancreatic master regulator PDX1 in cell lines with different degrees of differentiation of pancreatic cancer cells is accompanied by changes in the expression of known master genes involved in cancer progression. In BxPC3cells, as compared to BxPC3, we detected an increased expression of the following genes: NKX6.1 (2 times), NR5A2 (2.5 times), KLF5 (1.8 times), ZEB1 (3 times), and ONECUT1 (1.3 times), as well as a decreased expression of MUC1 and SLUG genes (3 and 2 times, respectively). In PANC1cells, as compared to the control PANC1cells, we detected a decreased expression of ISL1 (2 times) and an increased expressed of KRT8 (2 times) and MUC1 (by 30%). In the high-grade cell lines (including the BxPC3 line studied), the total content of sites containing the marks of active enhancers was higher than that in the low-grade cell lines (PANC1).
2537 related Products with: Dependence of expression of regulatory master genes of embryonic development in pancreatic cancer cells on the intracellular concentration of the master regulator PDX1.Ofloxacin CAS Number [824 DNA (cytosine 5) methyltr Glucagon ELISA KIT, Rat G Anti PDX1 Polyclonal Anti Thermal Shaker with cooli FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu MarkerGeneTM in vivo lacZ
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Glycoprotein 2 is a specific cell surface marker of human pancreatic progenitors.PDX1/NKX6-1pancreatic progenitors (PPs) give rise to endocrine cells both in vitro and in vivo. This cell population can be successfully differentiated from human pluripotent stem cells (hPSCs) and hold the potential to generate an unlimited supply of β cells for diabetes treatment. However, the efficiency of PP generation in vitro is highly variable, negatively impacting reproducibility and validation of in vitro and in vivo studies, and consequently, translation to the clinic. Here, we report the use of a proteomics approach to phenotypically characterize hPSC-derived PPs and distinguish these cells from non-PP populations during differentiation. Our analysis identifies the pancreatic secretory granule membrane major glycoprotein 2 (GP2) as a PP-specific cell surface marker. Remarkably, GP2 is co-expressed with NKX6-1 and PTF1A in human developing pancreata, indicating that it marks the multipotent pancreatic progenitors in vivo. Finally, we show that isolated hPSC-derived GP2cells generate β-like cells (C-PEPTIDE/NKX6-1) more efficiently compared to GP2and unsorted populations, underlining the potential therapeutic applications of GP2.Pancreatic progenitors (PPs) can be derived from human pluripotent stem cells in vitro but efficiency of differentiation varies, making it hard to sort for insulin-producing cells. Here, the authors use a proteomic approach to identify the secretory granule membrane glycoprotein 2 as a marker for PDX1+/NKX6-1+ PPs.
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[Fibroblast growth factors and their effects in pancreas organogenesis].Fibroblast growth factors (FGF) - growth factors that regulate many important biological processes, including proliferation and differentiation of embryonic cells during organogenesis. In this review, we will summarize current information about the involvement of FGFs in the pancreas organogenesis. Pancreas organogenesis is a complex process, which involves constant signaling from mesenchymal tissue. This orchestrates the activation of various regulator genes at specific stages, determining the specification of progenitor cells. Alterations in FGF/FGFR signaling pathway during this process lead to incorrect activation of the master genes, which leads to different pathologies during pancreas development. Understanding the full picture about role of FGF factors in pancreas development will make it possible to more accurately understand their role in other pathologies of this organ, including carcinogenesis.
2402 related Products with: [Fibroblast growth factors and their effects in pancreas organogenesis].Goat Anti-Human Fibroblas Fibroblast Growth Factor Fibroblast Growth Factor Fibroblast Growth Factor Fibroblast Growth Factor Human Insulin-like Growth Human Fibroblast Growth F Human Fibroblast Growth F Human Fibroblast Growth F Human Fibroblast Growth F Human Fibroblast Growth F Human Insulin-like Growth
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