EC Number   |
General Information |
Reference |
|---|
   1.14.11.2 | drug target |
C-P4H is a potential diagnostic marker and therapeutic target for cancer patients |
763830 |
| 1.14.11.2 | drug target |
targeting collagen P4H is a promising strategy to inhibit tumor progression and sensitize triple-negative breast cancer (TNBC) to chemotherapeutic agents. Inhibition of the enzyme (P4HA1) sensitizes triple-negative breast cancer (TNBC) to the chemotherapeutic agent docetaxel and doxorubicin in xenografts and patient-derived models. It is shown that increased P4HA1 expression correlates with short relapse-free survival in TNBC patients who received chemotherapy |
765458 |
| 1.14.11.2 | malfunction |
after 2 weeks of a treatment with lentivirus-mediated P4Halpha1 construct that is transfected in carotid plaque induced in mice (atherosclerotic plaques in ApoE-/- mice) by perivascular collar placement, both early and advanced plaque exhibit stable characteristics, with increased collagen and smooth muscle cell content, reduced macrophage content, and no change in lipid content. Lenti-P4Ha1 treatment of early and advanced plaque substantially increases interstitial collagen content in the fibrous cap of plaque. It increases the carotid plaque size and the relative en face lesion area of the aorta in early but not advanced plaque, with reduced phosphatase and tensin homologue expression. The treatment reduces the expression of inflammatory cytokines and the production and activity of matrix metalloproteinase-9 and -2 in both early and advanced plaque. P4Halpha1 overexpression has a differential effect at various stages of plaque pathological progression |
744826 |
| 1.14.11.2 | malfunction |
an Arabidopsis AtP4H3 T-DNA knock out mutant line shows higher sensitivity to anoxic treatment possibly due to lower induction of the fermentation pathway genes, ADH and PDC1, and of sucrose synthases, SUS1 and SUS4. This sensitivity to anoxia is accompanied by lower protein levels of AGPs-bound epitopes such as LM14 in the mutant line and induction of extensins-bound epitopes, while the expression levels of the majority of the AGPs genes are stable throughout a low oxygen time course. The lower AGPs content might be related to altered frequency of proline hydroxylation occurrence in the p4h3 line |
764785 |
| 1.14.11.2 | malfunction |
excessive collagen formation is involved in the pathogenesis of fibrosis, e.g. in liver and lung, resulting in abnormal wound healing and deformed tissue architecture |
695593 |
| 1.14.11.2 | malfunction |
knockout of either P4ha1 or P4ha2 greatly reduces LY83583-stimulated type I collagen maturation whereas silencing of both P4ha1 and P4ha2 completely blocks LY83583-induced type I collagen maturation |
764072 |
| 1.14.11.2 | malfunction |
mutations, where the hydrogen bonding network that involves the Tyr140 and Trp243 residues is disrupted, lead to major changes in folding of the protein and the size and shape of the substrate binding pocket. Trp243 mutation has major long-range effects |
745180 |
| 1.14.11.2 | malfunction |
overexpression of prolyl-4-hydroxylase-alpha1 stabilizes but increases shear stress-induced atherosclerotic plaque in apolipoprotein E-deficient mice. After 2 weeks of lenti-P4Halpha1 treatment both low and oscillatory shear stress-induced plaques increase collagen and the thickness of fibrous cap and decreases macrophage accumulation but show no change in lipid accumulation |
-, 744764 |
| 1.14.11.2 | malfunction |
pharmacologic or genetic inhibition of PHDs induces autophagy and prevents mammalian target of rapamycin complex 1 (mTORC1) activation by amino acids in a HIF-independent manner |
728416 |
| 1.14.11.2 | malfunction |
PHD1-/- mice have statistically non-significant reductions in infarct volumes following middle cerebral artery occlusion compared with their littermates at this time-point in this model |
728198 |
