CBX4 Antibody (Rabbit mAb) [P20K12]

Application: Reactivity: Mouse, Rat, Human

Usage Information

Dilution
WB1:1000 IP1:30 IHC1:200 FCM1:600 CHIP1:500

Application
WB, IP, IHC, FCM, ChIP

Reactivity
Mouse, Rat, Human

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 Observed MW
61 kDa 74 kDa, 75 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
CBX4 Antibody (Rabbit mAb) [P20K12] detects endogenous levels of total CBX4 protein.

Clone
P20K12

Synonym(s)
E3 SUMO-protein ligase CBX4, Chromobox protein homolog 4, Polycomb 2 homolog, Pc2, hPc2, CBX4

Background
CBX4, also known as chromobox protein homolog 4 or Polycomb 2, is a Polycomb-group protein that combines canonical chromatin-reading functions with SUMO E3 ligase activity, integrating epigenetic repression with post-translational modification to control gene expression programs linked to development, senescence and cancer progression. CBX4 is a nuclear protein containing an N‑terminal chromodomain that recognizes histone H3 trimethylated at lysine 27 and a C‑terminal region with SUMO-interacting motifs and RING-like features that confer SUMO E3 ligase activity; through its chromodomain, CBX4 binds H3K27me3-marked loci and recruits Polycomb Repressive Complex 1 (PRC1) components including BMI1 and RING1, promoting H2AK119 monoubiquitination and stable transcriptional repression at developmental and cell-cycle regulators. Beyond its role as a PRC1 reader and recruiter, CBX4 functions as a SUMO E3 ligase that modifies a range of substrates, including hypoxia-inducible factor 1α (HIF‑1α), thereby influencing their stability and activity. In hepatocellular carcinoma, CBX4 expression correlates with histologic grade, TNM stage, microvessel density and metastasis, and CBX4 enhances angiogenesis and metastatic potential by sumoylating HIF‑1α to increase its transcriptional activity on pro-angiogenic genes, with high CBX4 levels serving as an independent adverse prognostic factor and a biomarker guiding benefit from transarterial chemoembolization. In lung adenocarcinoma, CBX4 shows bidirectional transcriptional effects: it forms a CBX4/miR‑190 regulatory loop in which CBX4 represses miR‑190 to promote proliferation, while miR‑190 targets CBX4 to limit metastasis, and CBX4 also modulates expression of genes such as BMI1 and those controlling epithelial–mesenchymal transition, highlighting context-dependent roles in tumor growth versus dissemination. In gastric cancer, CBX4 is overexpressed and drives tumor progression and stemness by activating CDC20 and β‑catenin signaling, with CBX4 binding to regulatory regions and enhancing transcription of CDC20, which then supports cell-cycle progression, sphere formation and tumor-initiating capacity; CBX4 knockdown reduces proliferation, invasion and stemness markers, positioning CBX4 as a core epigenetic regulator of Wnt/β‑catenin and mitotic checkpoint networks in gastrointestinal malignancies. Outside of cancer, CBX4 contributes to senescence control: it represses p16INK4A expression through PRC1-mediated chromatin regulation and also sumoylates factors in senescence pathways, so that altered CBX4 activity can either delay or promote senescence and impact age-associated diseases, depending on tissue context and upstream signals.

Background

CBX4, also known as chromobox protein homolog 4 or Polycomb 2, is a Polycomb-group protein that combines canonical chromatin-reading functions with SUMO E3 ligase activity, integrating epigenetic repression with post-translational modification to control gene expression programs linked to development, senescence and cancer progression. CBX4 is a nuclear protein containing an N‑terminal chromodomain that recognizes histone H3 trimethylated at lysine 27 and a C‑terminal region with SUMO-interacting motifs and RING-like features that confer SUMO E3 ligase activity; through its chromodomain, CBX4 binds H3K27me3-marked loci and recruits Polycomb Repressive Complex 1 (PRC1) components including BMI1 and RING1, promoting H2AK119 monoubiquitination and stable transcriptional repression at developmental and cell-cycle regulators. Beyond its role as a PRC1 reader and recruiter, CBX4 functions as a SUMO E3 ligase that modifies a range of substrates, including hypoxia-inducible factor 1α (HIF‑1α), thereby influencing their stability and activity. In hepatocellular carcinoma, CBX4 expression correlates with histologic grade, TNM stage, microvessel density and metastasis, and CBX4 enhances angiogenesis and metastatic potential by sumoylating HIF‑1α to increase its transcriptional activity on pro-angiogenic genes, with high CBX4 levels serving as an independent adverse prognostic factor and a biomarker guiding benefit from transarterial chemoembolization. In lung adenocarcinoma, CBX4 shows bidirectional transcriptional effects: it forms a CBX4/miR‑190 regulatory loop in which CBX4 represses miR‑190 to promote proliferation, while miR‑190 targets CBX4 to limit metastasis, and CBX4 also modulates expression of genes such as BMI1 and those controlling epithelial–mesenchymal transition, highlighting context-dependent roles in tumor growth versus dissemination. In gastric cancer, CBX4 is overexpressed and drives tumor progression and stemness by activating CDC20 and β‑catenin signaling, with CBX4 binding to regulatory regions and enhancing transcription of CDC20, which then supports cell-cycle progression, sphere formation and tumor-initiating capacity; CBX4 knockdown reduces proliferation, invasion and stemness markers, positioning CBX4 as a core epigenetic regulator of Wnt/β‑catenin and mitotic checkpoint networks in gastrointestinal malignancies. Outside of cancer, CBX4 contributes to senescence control: it represses p16INK4A expression through PRC1-mediated chromatin regulation and also sumoylates factors in senescence pathways, so that altered CBX4 activity can either delay or promote senescence and impact age-associated diseases, depending on tissue context and upstream signals.

References
https://pubmed.ncbi.nlm.nih.gov/31724308/ https://pubmed.ncbi.nlm.nih.gov/25766328/

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%