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Anti-PDX1 Rabbit Antibody [E2L13]

Catalog No.: F3781

Application: Reactivity: Human, Mouse

Usage Information

Dilution
WB1:1000 IHC1:500

Application
WB, IHC, IF

Reactivity
Human, Mouse

Source
Rabbit

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
30 kDa 40 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight.

Positive Control	Human pancreas; Human duodenum; Human Colonic adenocarcinoma; Caco-2; Beta-TC-6
Negative Control	Human Heart muscle; Human brain; BxPC-3

Datasheet & SDS

Biological Description

Specificity
PDX1 Rabbit mAb detects endogenous levels of total PDX1 protein.

Clone
E2L13

Synonym(s)
IPF1, STF1, PDX1, Pancreas/duodenum homeobox protein 1, PDX-1, Glucose-sensitive factor, Insulin promoter factor 1, Insulin upstream factor 1, Islet/duodenum homeobox-1, Somatostatin-transactivating factor 1, GSF, IPF-1, IUF-1, IDX-1, STF-1

Background
The pancreatic duodenal homeobox gene-1 (PDX1) is a transcription factor that serves as a master regulator of pancreas development, pancreatic β-cell differentiation, and the maintenance of mature β-cell identity and function. During early embryonic development, PDX1 is expressed in pancreatic precursor cells and directs the commitment of endodermal cells toward a pancreatic fate. As the pancreas matures, its expression becomes largely restricted to β-cells, with lower levels found in certain δ-cells within the islets of Langerhans. PDX1 plays a pivotal role in transactivating genes essential for glucose sensing and metabolism, including the insulin gene, GLUT2, and glucokinase. Through these functions, it ensures proper insulin production and secretion in mature β-cells. Beyond the pancreas, PDX1 expression is also observed in the gastrointestinal tract (duodenum, stomach, pancreas) and in the central nervous system during development. Mutations in the PDX1 gene are linked to a range of pancreatic disorders. Homozygous loss-of-function mutations can result in pancreatic agenesis, while heterozygous mutations are associated with maturity-onset diabetes of the young type 4 (MODY4). In other forms of diabetes, PDX1 expression is often reduced. Loss of PDX1 function during development leads to arrested formation of the exocrine compartment and an underdeveloped endocrine compartment, as PDX1-expressing progenitors give rise to both pancreatic exocrine and endocrine lineages. This developmental arrest also impacts the NGN3-expressing progenitors that are essential for endocrine cell differentiation. Given its critical role in pancreas organogenesis, β-cell maturation, and insulin regulation, PDX1 is considered a central factor in both normal pancreatic function and the pathogenesis of pancreatic diseases.

Background

The pancreatic duodenal homeobox gene-1 (PDX1) is a transcription factor that serves as a master regulator of pancreas development, pancreatic β-cell differentiation, and the maintenance of mature β-cell identity and function. During early embryonic development, PDX1 is expressed in pancreatic precursor cells and directs the commitment of endodermal cells toward a pancreatic fate. As the pancreas matures, its expression becomes largely restricted to β-cells, with lower levels found in certain δ-cells within the islets of Langerhans. PDX1 plays a pivotal role in transactivating genes essential for glucose sensing and metabolism, including the insulin gene, GLUT2, and glucokinase. Through these functions, it ensures proper insulin production and secretion in mature β-cells. Beyond the pancreas, PDX1 expression is also observed in the gastrointestinal tract (duodenum, stomach, pancreas) and in the central nervous system during development. Mutations in the PDX1 gene are linked to a range of pancreatic disorders. Homozygous loss-of-function mutations can result in pancreatic agenesis, while heterozygous mutations are associated with maturity-onset diabetes of the young type 4 (MODY4). In other forms of diabetes, PDX1 expression is often reduced. Loss of PDX1 function during development leads to arrested formation of the exocrine compartment and an underdeveloped endocrine compartment, as PDX1-expressing progenitors give rise to both pancreatic exocrine and endocrine lineages. This developmental arrest also impacts the NGN3-expressing progenitors that are essential for endocrine cell differentiation. Given its critical role in pancreas organogenesis, β-cell maturation, and insulin regulation, PDX1 is considered a central factor in both normal pancreatic function and the pathogenesis of pancreatic diseases.

References
https://pubmed.ncbi.nlm.nih.gov/17938503/ https://pubmed.ncbi.nlm.nih.gov/36589234/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%