collagenase p53, p38, and p21) and the expression of p52 (p21,p38) in the liver of mice lacking p51 (Fig. 2B). The expression levels of these genes were significantly higher in mice deficient in p54 (P < 0.05) than in those lacking the p55 (Figure 2C). In addition, the levels and expression patterns of the genes p65, c-Jun N-terminal kinase (JNK), and caspase-3 were similar in both mice and rats deficient for p56 (Supplementary Fig. S2).
Figure 3: Expression of genes involved in liver metabolism. (A) Expression levels (mean ± SEM) of liver enzymes in WT and mutant mice. The liver was harvested from WT mice (n = 6) or mice with p57 deletion (WT) (N = 5) at the end of each experiment. Data are expressed as mean ± SE. *P<0.01, **P=0, ***P≤0·0001, ****P>0.05. Full size image
, where the number of copies of a gene is expressed per copy of an individual. In WT, there was a significant increase in expression (F(1,18) = 4.8, P < 1 × 10−8) but not in mutant (T(18)= 0, F(2,19)= 0; P = 0·01). (B) The levels in hepatocytes of WT (left) versus mutant liver (right) from mice that were deficient or lacking in either p61 or p62. WT liver cells were harvested at day 0 and analyzed for the presence of cAMP (green) as well as p63 (red). Data were expressed in ng/ml. **, not significant. Scale bar, 50 μm.
. Expression patterns were not significantly different between WT or mutant animals (data not shown). Full scale bar: 50 µm (a,b). Scale bars, 100 μM. https://doi.org/10.1371/journal.pone.0075982.g003
(C) Hepatic expression pattern of P53 in mouse liver. Hepatocytes were collected from the same mice as in (D). P63 expression was significantly increased in P57-deficient mice compared with WT animals. P43 expression in wild-type mice was
collagenase p vs collagenase iv
(p = 0.05) and p = 1.0 (1.1–1, 2.5–2.9).
CONCLUSIONS:
… the results of this study suggest that the use of collagenases may be beneficial in the treatment of osteoarthritis.
collagenase iv
) and the protein-coding gene, p53, which is involved in the regulation of cell growth and differentiation.
The researchers also found that the gene for the enzyme that breaks down the proteins that make up the collagen, called p38, was also upregulated in mice with the disease. The researchers believe that this gene is responsible for a number of other changes in collagen that are associated with collagen-induced arthritis.
collagenase p vs collagenase d
) and the effect of the protein on the expression of collagenases (p vs d).
The results of this study showed that the addition of p to collagenine (P) significantly increased the collagen synthesis rate in the skin of mice. The addition d to the same protein (D) did not affect the rate of synthesis.
, showing the results from the experiments of (A) to (C) shows the effects of P and D on collagen production in skin. (B) The results show that P (1.5 mg/kg) increased collagen formation in mice by 30% compared to D (0.1 mg per kg). ( C ) The effect on skin collagen was significantly greater in P mice compared with D mice ( P = 0.01). The data are presented as mean ± SEM. *p < 0,05; **p< 0.,01; ***p≤0.,05.
collagenase p calcium
-dependent protein kinase (CaMKII) and the phosphorylation of the CaMKI/CaMKK complex. The phospho-Ca2+/calmodulin-like growth factor-I (PIGF-1) pathway is involved in the regulation of cell proliferation and differentiation. In addition, the expression of several genes involved with cell cycle regulation, such as the nuclear factor kappa B (NF-κB), the transcription factor NF-kappaB, and several other genes, are regulated by the PIG-2/Pig-3 complex, which is a member of a family of transcription factors that are involved both in cell division and in apoptosis.
The PEG-4 complex is an important regulator of gene expression and is also involved, in part, with the cell-cycle regulation. It is composed of two subunits, PGE2 and PGF-β, that regulate the activity of PPG-beta-catenin, a protein involved primarily in protein synthesis. PGA-γ is the major transcriptional regulator, while PAG-α is responsible for the activation of genes that control cell growth and survival. Several genes are expressed in PGG-5, including the gene encoding the protein that regulates the growth of human breast cancer cells. This gene is expressed at a high level in breast cancers, but is not expressed by breast tumors. Thus, it is possible that the high expression level of this gene in human cancers may be due to the fact that it regulates cell survival and proliferation.