ERG Antibody [N14M7] | Primary Antibodies

Application: Reactivity: Human, Mouse

Lane 1: MOLT-4

Usage Information

Dilution
WB1:1000 IP1:100 IHC1:200 IF1:500 FCM1:50

Application
WB, IP, IHC, IF, FCM

Reactivity
Human, Mouse

Source
Rabbit Monoclonal Antibody

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
54 kDa

Datasheet & SDS

Biological Description

Specificity
ERG Antibody [N14M7] detects endogenous levels of total ERG protein.

Clone
N14M7

Synonym(s)
Transcriptional regulator ERG; Transforming protein ERG; ERG

Background
ERG belongs to the ETS family of transcription factors, which bind specific DNA sequences to control gene expression during development and cell growth. It has a key ETS DNA-binding domain at the C-terminus and an N-terminal region that activates transcription through interactions with other proteins. ERG drives gene programs by binding ETS motifs in promoters and enhancers, often partnering with RUNX1 to co-occupy chromatin and activate endothelial genes such as VEGFR2 and Tie2, while repressing others through epigenetic silencing via histone deacetylases. ERG integrates signals from VEGF/PI3K pathways to maintain vascular integrity, promoting junctional remodeling via VE-cadherin regulation and shear-stress responses that fine-tune arterial-venous specification in endothelial cells. During hematopoiesis, ERG sustains stem cell pluripotency by counteracting differentiation cues from GATA2 and FLI1, ensuring balanced output of erythroid, myeloid, and megakaryocytic lineages. This dual role in vascular and blood development makes ERG essential for studying tissue specification where lineage fidelity meets environmental cues. Chromosomal fusions like EWSR1-ERG in Ewing sarcoma hijack ERG's pointed domain for aberrant super-enhancer formation, driving IGF1R/GLI1 expression and sarcomagenesis, while TMPRSS2-ERG fusions in prostate cancer amplify androgen-driven proliferation through MYC/AR pathway hijacking and PTEN loss synergy. Normal ERG expression persists in adult endothelial beds, with post-translational control via MAPK phosphorylation modulating its activity in angiogenesis and inflammation.

Background

ERG belongs to the ETS family of transcription factors, which bind specific DNA sequences to control gene expression during development and cell growth. It has a key ETS DNA-binding domain at the C-terminus and an N-terminal region that activates transcription through interactions with other proteins. ERG drives gene programs by binding ETS motifs in promoters and enhancers, often partnering with RUNX1 to co-occupy chromatin and activate endothelial genes such as VEGFR2 and Tie2, while repressing others through epigenetic silencing via histone deacetylases. ERG integrates signals from VEGF/PI3K pathways to maintain vascular integrity, promoting junctional remodeling via VE-cadherin regulation and shear-stress responses that fine-tune arterial-venous specification in endothelial cells. During hematopoiesis, ERG sustains stem cell pluripotency by counteracting differentiation cues from GATA2 and FLI1, ensuring balanced output of erythroid, myeloid, and megakaryocytic lineages. This dual role in vascular and blood development makes ERG essential for studying tissue specification where lineage fidelity meets environmental cues. Chromosomal fusions like EWSR1-ERG in Ewing sarcoma hijack ERG's pointed domain for aberrant super-enhancer formation, driving IGF1R/GLI1 expression and sarcomagenesis, while TMPRSS2-ERG fusions in prostate cancer amplify androgen-driven proliferation through MYC/AR pathway hijacking and PTEN loss synergy. Normal ERG expression persists in adult endothelial beds, with post-translational control via MAPK phosphorylation modulating its activity in angiogenesis and inflammation.

References
https://pubmed.ncbi.nlm.nih.gov/26690869/ https://pubmed.ncbi.nlm.nih.gov/23264855/

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

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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%