Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One neurofibrosarcoma from each of three patients with von Recklinghausen neurofibromatosis (VRNF) was studied for the expression of selected growth factor genes and oncogenes. Comparative analyses were also performed on four neurofibromas and skin, nerve and muscle specimens from one of the patients with neurofibrosarcoma, an autopsy kidney specimen from a fifth VRNF patient, and normal liver and term placenta specimens from healthy control subjects. Northern blot hybridization techniques were used to analyze the amounts and sizes of mRNA resulting from the expression of eight genes. Insulin-like growth factor I showed a moderate level of expression in normal nerve and lower expression in two neurofibrosarcomas. Insulin-like growth factor II was moderately to heavily expressed in all specimens, and differential splicing patterns were seen. Platelet-derived growth factor showed low levels of expression in all three neurofibrosarcomas, skin, nerve, muscle and normal liver, low to moderate levels of expression in the neurofibromas, and high expression in normal control placenta. Beta-nerve growth factor was expressed at low levels in two neurofibrosarcomas and skin, but was not seen in other specimens. N-myc showed a low level of expression in one neurofibrosarcoma and a neurofibroma, and a higher level of expression in a second neurofibrosarcoma (and in this same subject's skin and nerve). Tissue-type plasminogen activator showed moderate levels of expression in two neurofibrosarcomas and one neurofibroma, but it was not seen in skin, nerve, kidney and normal term placenta specimens.
 ...
PMID:Expression of selected growth factors and oncogenes in neurofibrosarcomas complicating von Recklinghausen disease. 315 36

The aim of this study was to determine whether enhanced expression of N-myc in a neuroblastoma cell line affects the balance of plasminogen activator/plasminogen activator inhibitor (PA/PAI), a shift towards proteolysis having been observed in other malignant tissues. Two transfected neuroblastoma cell lines with (WAC2 cells) or without (SH-EP007 cells) enhanced expression of the N-myc oncogene were examined by zymography and RNA extraction to determine UPA and PAI enzyme activity and uPA RNA and PAI RNA expression, respectively. The effect of genistein, an inhibitor of tyrosine protein kinase, on uPA/PAI was also investigated. Both the uPA/PAI-1 ratio at mRNA level and the PA/PAI ratio at protein activity level were higher in the more malignant, WAC2 cell line. Genistein attenuated uPA activity and stimulated PAI activity in both cell lines, leading to a decrease in the PA/PAI ratio. This effect was more pronounced in the more malignant, WAC2 cell line.
 ...
PMID:Modulation of the proteolytic balance plasminogen activator/plasminogen activator inhibitor by enhanced N-myc oncogene expression or application of genistein. 989 62

Glutamate receptors play an important role in the function of astrocytes. Among their tasks is the regulation of gliotransmission, gene expression and exocytosis of the tissue-type plasminogen activator (tPA), which has an enhancing effect on N-methyl-D-aspartate (NMDA) receptors and thus prevent over-excitation of neighboring neurons. The kainate receptor GluK2, which is expressed in neurons and astrocytes, is under tight regulation of the PI3-kinase SGK pathway as shown in neurons. SGK1 targets include N-myc downstream-regulated genes (NDRGs) 1 and 2 (NDRG1, NDRG2), proteins with elusive function. In the present study, we analyzed the effects of SGK1, NDRG1, and NDRG2 on GluK2 current amplitude and plasma membrane localization in astrocytes and heterologous expression. We demonstrate that NDRG1 and NDRG2 themselves have no effect on GluK2 current amplitudes in heterologous expressed ion channels. However, when NDRG2 is coexpressed with GluK2 and SGK1, the stimulating effect of SGK1 on GluK2 is suppressed both in heterologous expression and in astrocytes. Here, we reveal a new negative feedback mechanism, whereby GluK2 stimulation by SGK1 is regulated by parallel phosphorylation of NDRG2. This regulation of GluK2 by SGK1 and NDRG2 in astrocytes may play an important role in gliotransmission, modulation of gene expression and regulation of exocytosis of tPA.
...
PMID:NDRG2 phosphorylation provides negative feedback for SGK1-dependent regulation of a kainate receptor in astrocytes. 2650 Apr 92