Disease relevance of PCNA

• PCNA appeared not only in the supporting cells, as indicated in previous studies, but also in the ganglion cells, suggesting ganglion cell involvement in the process of regeneration [1].
• Resection type, proliferation markers (Ki67 and PCNA) and in vitro confrontation patterns were significant (p<0.05) factors in predicting the postsurgical evolution of meningiomas [2].

High impact information on PCNA

• Here, MCMT is shown to bind proliferating cell nuclear antigen (PCNA), an auxiliary factor for DNA replication and repair [3].
• p21(Cip1/WAF1) has cell cycle inhibitory activity by binding to and inhibiting both cyclin/Cdk kinases and proliferating cell nuclear antigen [4].
• This effect on proliferation was corroborated by the finding that the percentage of exogenous Gax-expressing myocytes that were positive for the cell cycle marker PCNA decreased over time and was lower than in control myocytes [5].
• Cell proliferation in the gastrulating chick embryo: a study using BrdU incorporation and PCNA localization [6].
• Immunocytochemical localization of PCNA-positive nuclei gave generally similar distributions to those obtained with BrdU incorporation, confirming that this endogenous molecule is a useful S-phase marker during early embryogenesis [6].

Biological context of PCNA

• Co-localization of chicken DNA topoisomerase IIalpha, but not beta, with sites of DNA replication and possible involvement of a C-terminal region of alpha through its binding to PCNA [7].
• Indeed, the monoubiquitination-defective Proliferating Cell Nuclear Antigen (PCNA) mutant exhibits impaired recombination-independent ICL repair as well as drastically reduced mutation rate, indicating that the PCNA switch is utilized to enable lesion bypass during DNA repair synthesis [8].
• Moreover, challenge of ovarian granulosa cells with ghrelin 1-18 was able to induce markers of proliferation (i.e. expression of both PCNA and cyclin), and to modulate markers of apoptosis (i.e. decreased expression of caspase-3, bax, bcl-2 and TUNEL-positive cells) [9].
• The frequency of PCNA-positive cells started to increase from 7 d after cessation of lay (3 d after refeeding), and a significantly higher frequency of positive cells was observed in both lobes of molting hens 13 d after cessation of lay when compared to control hens, molting hens 2 d after cessation of egg lay, and second cycle laying hens [10].
• The cell number and total DNA were significantly larger and the level of LDH and proliferating cell nuclear antigen (PCNA) was elevated in Ca/2 compared to FCa [11].

Anatomical context of PCNA

• The number of germ cells was counted and the proliferating cells were identified by immunocytochemistry of proliferating cell nuclear antigen (PCNA) [12].
• As with BrdU incorporation, the highest proportions of PCNA-positive nuclei were found towards the caudal regions of the epiblast and mesoderm [6].
• Increased expression of PCNA and decreased expression of neuronal class III beta-tubulin were observed in the spinal cord after anti-CL-PSP IgG injection [13].
• The cell proliferation and differentiation of the epithelial cells of the epididymis were evaluated with the use of the monoclonal antiproliferating cell nuclear antigen (PCNA-cyclin) antibody, and the AE1 keratin complex antibody [14].
• If, however, the organ cultures were wounded, allowing the RPE cells to spread and migrate over the exposed basal lamina, the nuclei of cells along the wound edge were stained for PCNA [15].

Associations of PCNA with chemical compounds

• Moreover, ghrelin 1-18 increased the expression of PCNA, cyclin, bax and p53 in cultures of ovarian follicular fragments, where it also stimulated the release of progesterone, estradiol, arginine-vasotocin (AVT) and IGF-I, but not of testosterone [9].
• We found that cells at the peripheral edge of the retina incorporated the thymidine analog BrdU and expressed the cell cycle regulator proliferating cell nuclear antigen (PCNA) [16].
• In addition, we applied morphogens, such as fibroblast growth factors (FGFs), bone morphogenetic proteins (BMPs), and retinoic acid (RA), and subsequently analyzed changes in the pattern of PCNA expression [17].
• MATERIALS AND METHODS: We investigated chick embryos of Hamburger and Hamilton stages 16-45 by staining for proliferating cell nuclear antigen (PCNA) and applying the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) method [18].

Other interactions of PCNA

• Dual immunohistochemical staining results showed that almost all the Lim-3(+)cells expressed Islet-1 at every stage examined, and about 90% of Islet-1(+)cells were proliferating cell nuclear antigen negative [19].
• Twelve hours to 1 day after exposure, mitotic cells, binucleate cells and PCNA-positive supporting cells were observed, and b-FGF immunoreactivity was shown in the supporting cells and glial cells near the habenula perforata [20].
• Immunodetection of PCNA, a marker of cell proliferation, revealed a much more widespread distribution of mitotic cells as compared to CHox-cad-expressing cells [21].

Analytical, diagnostic and therapeutic context of PCNA

• Compared with the control group, the surgery group showed a lower PCNA labeling index for 5 days after surgery and demonstrated more TUNEL-positive cells at 6 h, 3 and 5 days after surgery [22].
• Cytokinetic pattern in the thoracic spinal cord of chick embryos (incubation day 5-13) using PCNA staining and TUNEL method [23].
• Conversely, PCNA was not expressed by RPE cells of the same age maintained in organ culture [15].
• Frequency of proliferating cells and immunoreactive CaBP-D28K molecules were identified by immunocytochemistry for proliferating cell nuclear antigen (PCNA) and Western blot for CaBP-D28K [24].
• PCNA in situ hybridization: a novel and reliable tool for detection of dynamic changes in proliferative activity [17].

References