UBR5 Antibody [A19C24] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat, Monkey

Lane 1: HT1080, Lane 2: MCF7, Lane 3: SH-SY5Y, Lane 4: COS-7

Usage Information

Dilution
WB1:1000 IP1:50

Application
WB, IP

Reactivity
Human, Mouse, Rat, Monkey

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
300 kDa

Datasheet & SDS

Biological Description

Specificity
UBR5 Antibody [A19C24] detects endogenous levels of total UBR5 protein.

Clone
A19C24

Synonym(s)
E3 ubiquitin-protein ligase UBR5; E3 ubiquitin-protein ligase, HECT domain-containing 1; Hyperplastic discs protein homolog; hHYD; Progestin-induced protein; UBR5; EDD; EDD1; HYD; KIAA0896

Background
UBR5, a HECT-domain E3 ubiquitin ligase within the N-recognin family of the N-end rule pathway, orchestrates targeted protein degradation to maintain cellular signaling homeostasis through its UBR and WWE domains that flank the catalytic HECT lobe for precise substrate recognition. In the DNA damage response, UBR5 ubiquitinates RNF8 and RNF168 to restrict their accumulation at double-strand breaks, preventing excessive H2A/H2AX ubiquitination while enabling controlled 53BP1 recruitment through RNF168 turnover, thereby integrating with ATM/CHK2 signaling and stabilizing TopBP1 to support replication fork progression. Loss of UBR5 triggers RNF168 hyperaccumulation, fork collapse, and hypersensitivity to doxorubicin due to homologous recombination defects involving RAD51 and BRCA1. In triple-negative breast cancer, UBR5 drives aggressive progression by polyubiquitinating E-cadherin for lysosomal degradation, thereby activating β-catenin/TCF-mediated transcription that fuels proliferation, angiogenesis, and lung metastasis, even as it paradoxically recruits CD8+ T cells via type I interferon signaling without curbing tumor outgrowth. UBR5 fine-tunes Th17 cell differentiation by targeting RORγt for proteasomal degradation, counterbalancing DUBA-mediated deubiquitination to limit IL-17-driven intestinal inflammation. UBR5 links proteostasis to epithelial and neuronal cell polarity via N-degron substrates, with its amplification correlating to poor survival in breast and ovarian cancers owing to pro-metastatic roles in polarized contexts.

Background

UBR5, a HECT-domain E3 ubiquitin ligase within the N-recognin family of the N-end rule pathway, orchestrates targeted protein degradation to maintain cellular signaling homeostasis through its UBR and WWE domains that flank the catalytic HECT lobe for precise substrate recognition. In the DNA damage response, UBR5 ubiquitinates RNF8 and RNF168 to restrict their accumulation at double-strand breaks, preventing excessive H2A/H2AX ubiquitination while enabling controlled 53BP1 recruitment through RNF168 turnover, thereby integrating with ATM/CHK2 signaling and stabilizing TopBP1 to support replication fork progression. Loss of UBR5 triggers RNF168 hyperaccumulation, fork collapse, and hypersensitivity to doxorubicin due to homologous recombination defects involving RAD51 and BRCA1. In triple-negative breast cancer, UBR5 drives aggressive progression by polyubiquitinating E-cadherin for lysosomal degradation, thereby activating β-catenin/TCF-mediated transcription that fuels proliferation, angiogenesis, and lung metastasis, even as it paradoxically recruits CD8+ T cells via type I interferon signaling without curbing tumor outgrowth. UBR5 fine-tunes Th17 cell differentiation by targeting RORγt for proteasomal degradation, counterbalancing DUBA-mediated deubiquitination to limit IL-17-driven intestinal inflammation. UBR5 links proteostasis to epithelial and neuronal cell polarity via N-degron substrates, with its amplification correlating to poor survival in breast and ovarian cancers owing to pro-metastatic roles in polarized contexts.

References
https://pubmed.ncbi.nlm.nih.gov/34635393/ https://pubmed.ncbi.nlm.nih.gov/28330927/

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%