Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.35 (matrix metalloproteinase 9)
 2,207 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The v-erbA oncogene coding for a mutated form of the thyroid hormone (T3) receptor (TR alpha 1) increased the invasion capacity of the mouse B3.1 glial cell line. This effect was mediated by the induction of platelet-derived growth factor (c-sis/PDGF B), as shown by its inhibition using an anti-PDGF BB antibody. Also, the low invasion capacity of parental B3.1 and c-erbA-expressing cells (B3.1 + TR alpha 1) was enhanced by exogenously added PDGF BB. This effect was independent of the growth-promoting activity of PDGF and unrelated to the secretion of metalloproteinases. All three cell types (parental B3.1, B3.1 + v-erbA, and B3.1 + TR alpha 1) secreted similar high levels of the M(r) 72,000 collagenase IV (A) independently of PDGF. Anchorage-independent cell growth was also enhanced by v-erbA; B3.1 + v-erbA cells but neither parental B3.1 nor B3.1 + TR alpha 1 cells formed foci in soft agar. The effect of v-erbA only happened in the presence of serum, suggesting that some serum factor(s) cooperate with PDGF to overcome the anchorage dependence of B3.1 + v-erbA cells. Supporting this, high doses of exogenous PDGF were much less efficient than serum, and the addition of an anti-PDGF BB antibody blocked only partially the effect of serum. Basic fibroblast growth factor was found to cooperate with PDGF to abolish anchorage dependence. Moreover, B3.1 + v-erbA cells detached and grew in suspension when cultured on plastic dishes. Interestingly, the transformation-competent c-jun and fra-1 oncogenes were induced by v-erbA in serum-free medium and are candidates to mediate v-erbA effects. In summary, our results show that v-erbA induces transformation parameters in the glial B3.1 cell line via an increase in c-sis/PDGF B and probably other mechanisms, suggesting a role for (autocrine) PDGF stimulation in glial cell transformation.
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PMID:v-erbA oncogene induces invasiveness and anchorage-independent growth in cultured glial cells by mechanisms involving platelet-derived growth factor. 883 67

Presently in the environment, there exist a number of chemical contaminants which share structural similarity with key naturally occurring regulatory hormones. These hormones play pivotal roles in the normal growth and development of wildlife species and humans. In particular, biphenolic chemical compounds may have the potential to act as agonists or antagonists of thyroid hormone (TH) action. We investigated whether there was any biological effect of exposure to low concentrations of the brominated fire retardant, tetrabromobisphenol-A (TBBPA), on the TH-mediated process of metamorphosis of the Pacific tree frog, Pseudacris regilla. Tadpoles exposed to 10nM (5.4microg/L) TBBPA showed an increase in TH-mediated expression of gelatinase B mRNA within 48h in the tadpole tail which was associated with increased tail resorption by 96h. Treatment with 100nM (54.4microg/L) TBBPA resulted in increased TH-mediated thyroid hormone receptor alpha mRNA expression in the tadpole brain and reduced levels of PCNA transcript in the tail. TBBPA alone was also found to alter the mRNA abundance of thyroid hormone receptor alpha in tail, gelatinase B in brain, and PCNA in both tissues of premetamorphic tadpoles. Interestingly, expression of thyroid hormone receptor beta mRNA was not affected by exposure to TBBPA either alone or in the presence of TH. The results suggest that exposure to low levels of TBBPA may act as an agonist of TH action and potentiate TH-mediated gene expression leading to accelerated anuran metamorphosis.
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PMID:Exposure to tetrabromobisphenol-A alters TH-associated gene expression and tadpole metamorphosis in the Pacific tree frog Pseudacris regilla. 1667 81