anti-Prolyl 4-Hydroxylase, alpha Polypeptide I (P4HA1) Antibodies

Mouse (Murine) Prolyl 4-Hydroxylase, alpha Polypeptide I (P4HA1) interaction partners

1. Overexpression of P4Ha1 increased atherosclerotic plaque size.

2. Impaired extracellular matrix is the primary cause of death of C-P4H-I+/-;C-P4H-II-/- growth plate chondrocytes.

3. IL-6 destabilizes atherosclerotic plaques by downregulating P4Halpha1 via an RAF-MEK1/2-ERK1/2 MAPK and c-Jun pathway.

4. C-P4H alpha(I) and alpha(II) mRNA levels were increased in hypoxic mouse chondrocytes in a manner dependent on HIF-1a.

Human Prolyl 4-Hydroxylase, alpha Polypeptide I (P4HA1) interaction partners

1. Collagen prolyl 4-hydroxylase alpha 1 subunit (P4HA1) protein expression is induced in triple-negative breast cancer (TNBC) and HER2 positive breast cancer. Inhibition of P4HA1 sensitizes TNBC to the chemotherapeutic agent docetaxel and doxorubicin in xenografts and patient-derived models. Increased P4HA1 expression correlates with short relapse-free survival in TNBC patients who received chemotherapy.

2. miR-122 inhibited migration, invasion, epithelial mesenchymal transition, and metastasis in peritoneal cavity of ovarian cancer cells by targeting P4HA1.

3. High expression of P4HA1 was correlated with the malignancy of gliomas and could serve as a prognostic indicator for patients with high-grade gliomas

4. Our study indicates that P4HA1 plays a pivotal role in the process of GSC-EC transdifferentiation and the structural formation of vascular BMs.

5. we report compound heterozygous frameshift and splice site mutations in P4HA1 that impair but not abolish C-P4H alpha(I) activity. The maternal P4HA1 exon 12 splice donor site mutation causes an internally deleted C-P4H alpha(I) predicted to completely lack catalytic activity. two nucleic acid insertion in exon 9 results in a premature stop in the exon 9 P4HA1 splice form.

6. Findings suggest that the catalytic domain of collagen prolyl 4-hydroxylases (CP4Hs) recognizes the cis conformation of the prolyl peptide bond.

7. Thus, we conclude that miR-30e suppresses proliferation of hepatoma cells through targeting P4HA1 mRNA.

8. Studies indicate P4HA1 copy number gain in a subset of metastatic prostate tumors and its expression is also regulated by microRNA-124.

9. Overexpression of miR-122 markedly attenuated the expression of P4HA1 via targeting a binding site located at 3'-UTR of P4HA1 mRNA

10. Hypoxia-inducible factor 1 (HIF-1) promotes extracellular matrix remodeling under hypoxic conditions by inducing P4HA1, P4HA2, and PLOD2 expression in fibroblasts.

11. IL-6 significantly downregulated P4Halpha1 expression in aortic smooth muscle cells

12. analysis of the 2-His-1-Asp active-site motif in prolyl 4-hydroxylase

13. These in vivo data demonstrated that smokers had thinner atherosclerotic cap thickness and lower levels of P4Halpha and collagen.

14. Collagen prolyl 4-hydroxylase-alpha (I)mRNA is stabilized by interation of RNA-binding proteins hnRNP-A2/B1 with a U(16) element within the 3'-UTR

15. positive (transforming growth factor beta1) and negative (cigarette smoking extract) regulators appear to influence the USF-E-box interaction and affect P4Halpha(I) expression

16. Results suggest that the alteration of translational efficiency by nucleolin, which occurs through a hypoxia inducible factor independent pathway, is an important step in collagen prolyl 4-hydroxylase-alpha(I) regulation under hypoxia.

17. In comparison with healthy cartilage, Osteoarthritis articular chondrocytes exhibit increased in vivo synthesis of collagen prolyl-4-hydroxylase type II, a pivotal enzyme in collagen triple helix formation.

18. HIF-P4H, HIF-1alpha and HIF-2alpha are effective oxygen sensors