Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q9UIJ5 (Rec)
 58,342 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Deer antlers are the only mammalian appendage to display an annual cycle of full regeneration. The growth phase in antler involves the rapid proliferation of several tissues types, including epidermis, dermis, cartilage, bone, blood vessels, and nerves. Antlers thus provide an excellent model to study the developmental regulation of these tissues. We describe here the identification of two genes, pigment epithelium-derived factor (PEDF) and cyclin-dependent kinase inhibitor 1C (CDKN1C), both of which are known to be involved in cell proliferation and differentiation. These genes were identified as the result of screening an expressed sequence tag database derived from a cDNA library enriched for sequences from the growing antler tip. PEDF mRNA was detected in developing skin, cartilage, and bone during endochondral ossification. PEDF mRNA was not detected within endothelial cells that exhibited positive immunoreactivity to a CD146 antibody. CDKN1C mRNA was expressed by only the immature chondrocytes within the precartilage region. These results suggested that PEDF and CDKN1C are important genes involved in cell proliferation and differentiation during antler growth.
Anat Rec (Hoboken) 2007 Aug
PMID:Cell cycle genes PEDF and CDKN1C in growing deer antlers. 1761 Feb 57

The p21-activated kinases have been implicated in the control of cell cycle progression. However, the biological mechanism underlying the role of p21-activated kinase 4 (PAK4) in cell cycle control remains unknown. Here, by using quantitative RT-PCR and immunoblot analyses, we discovered that over-expression of PAK4 could suppress cyclin-dependent kinase inhibitor 1C (p57(Kip2) ) expression in the MCF-7 human breast cancer cell line, whereas lentiviral vector-mediated small interfering RNA (siRNA) knockdown of PAK4 markedly promoted p57(Kip2) expression in MCF-7 cells. Furthermore, PAK4-mediated down-regulation of p57(Kip2) was reversed by MG132, a specific proteasome inhibitor. The ubiquitination assay confirmed that the activity of PAK4 attenuated p57(Kip2) protein stability through the ubiquitin-proteasome pathway in MCF-7 cells. Moreover, a significant inverse correlation between PAK4 and p57(Kip2) protein levels was observed in breast cancer tissues by immunohistochemical analysis. Taken together, our data demonstrate a novel function for PAK4 in regulating the stability of p57(Kip2) , possibly through the ubiquitin-proteasome pathway, leading to increased proliferation of breast cancer cells. Thus, PAK4 may be used as a potential diagnostic and therapeutic target for human breast cancer.
Anat Rec (Hoboken) 2013 Oct
PMID:P21-activated kinase 4 regulates the cyclin-dependent kinase inhibitor p57(kip2) in human breast cancer. 2387 32