anti-PR Domain Containing 5 (PRDM5) Antibodies

Human PR Domain Containing 5 (PRDM5) interaction partners

1. Inhibiting PRDM5 expression by siRNA attenuated the IFN-gamma-triggered accumulation of active caspase-3 and cleaved PARP in intestinal epithelial cells. Moreover, flow cytometry assay and CCK-8 analysis revealed that PRDM5 knockdown significantly alleviated the IFN-gamma-induced cellular apoptosis in HT29 cells.

2. Both Prdm 4 and Prdm 5 are expressed in human corneal endothelium, primary hCECs and in HCECs-12 cells, characterised by expression of the Na(+)/K(+)-ATPase.

3. The miR-182 promoter is rarely methylated in epithelial ovarian cancers (EOCs), and its methylation status is associated with lower miR-182 expression. Deletion of the PRDM5 locus may play a supportive role in miR-182 overexpression in EOC. miR-182 is an unfavorable prognostic factor in EOC.

4. The current study revealed a novel mutation in the PRDM5 gene in a Brittle cornea syndrome (BCS) family and recurrent mutation in a sporadic BCS patient.

5. Genetic variants in PRDM5 can lead to various syndromic and nonsyndromic disorders affecting the anterior segment of the eye.

6. Defective interaction of PRDM5 with repressive complexes, and dysregulation of H3K9me2, play a role in PRDM5-associated disease.

7. Reduced expression of PRDM5 was observed in the cornea and retina of brittle cornea syndrome patients.

8. These data suggest that PRDM5 is a relevant tumour suppressor gene that is frequently targeted in colorectal tumourigenesis.

9. PRDM2, PRDM5, PRDM16 promoters are methylated and their expression is suppressed in lung cancer cells.

10. Data provide the first causal link between Prdm5 loss and intestinal carcinogenesis, and uncover an extensive and novel PRDM5 target repertoire likely facilitating the tumor-suppressive functions of PRDM5.

11. Promoter methylation-mediated downregulation of PRDM5 contributes to the development of lung squamous cell carcinoma.

12. Frequent epigenetic silencing of PRDM5 is involved in multiple tumorigeneses, which could serve as a tumor biomarker

13. ZNF469 and PRDM5, two genes that when mutated cause brittle cornea syndrome, participate in the same regulatory pathway.

14. Data show that reduced expression of PRDM5 may play an important role in the pathogenesis and/or development of cervical cancer, and is considered to be caused in part by aberrant DNA methylation.

15. PRDM5 caused G2/M arrest and apoptosis upon infection of tumor cells. These results suggest that inactivation of PRDM5 may play a role in carcinogenesis.

16. Results identify PRDM5, which acts as a sequence-specific, DNA binding transcription factor that targets hematopoiesis-associated protein-coding and microRNA genes, some of which are targets of Gfi1.

17. Data suggest that epigenetic alteration of PRDM5 (e.g., methylation of its 5'-CpG island or trimethylation of Lys(27) of histone H3) likely plays a key role in the progression of gastrointestinal cancers and may be a useful molecular marker.

Zebrafish PR Domain Containing 5 (PRDM5) interaction partners

1. Prdm5 is expressed specifically in the area of the forming neurocranium during craniofacial development.

2. PRDM5 regulates the expression of components of both canonical and non canonical wnt pathways and negatively modulates wnt signaling in vivo

Mouse (Murine) PR Domain Containing 5 (PRDM5) interaction partners

1. PRDM5 promotes the proliferation and invasion of murine melanoma cells through up-regulating JNK expression and strategies targeting PRDM5 may be promising for the therapy of melanoma.

2. Data provide the first causal link between Prdm5 loss and intestinal carcinogenesis, and uncover an extensive and novel PRDM5 target repertoire likely facilitating the tumor-suppressive functions of PRDM5.

3. These data indicate how Prdm5 modulates transcription by interacting with factors involved in genome organization in mouse embryonic stem cells.

4. we show that Prdm5 controls both Collagen I transcription and fibrillogenesis by binding inside the Col1a1 gene body and maintaining RNA polymerase II occupancy