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Query: UNIPROT:P17931 (galectin-3)
 2,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Galectin-3, a member of the galectin family of beta-galactoside-specific lectins has been found to be expressed by subsets of dorsal root ganglion (DRG) neurons during development and in adulthood. Here we show that (i) after 3-7 days in vitro, DRG neurons derived from neonatal mice express galectin-3 intra- and extracellularly and (ii) lectin expression requires the presence of nerve growth factor (NGF). After 3 days in vitro, a higher number of DRG neurons expressed galectin-3 in the presence of NGF (65 +/- 7%) than in the presence of brain-derived neurotrophic factor (BDNF, 30 +/- 3%) or neurotrophin-3 (NT-3, 34 +/- 3%). After 7 days in vitro, these numbers dropped to 51 +/- 3% (for NGF), 0% (for BDNF) and 8 +/- 4% (for NT-3), respectively. Our findings provide first evidence for the contribution of a neurotrophin to the neuronal expression of galectins and suggest an NGF/TrkA-mediated expression of galectin-3 by early postnatal DRG neurons.
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PMID:Nerve growth factor-mediated expression of galectin-3 in mouse dorsal root ganglion neurons. 1106 32

Galectin-3 (gal-3) is a member of the galectin family of lectins whose expression strongly depends on the cellular state. Here we show that in PC12 cells the expression of gal-3 protein is regulated via Ras- and mitogen-activated protein kinase (MAPK)-dependent and independent signalling pathways and correlates with nerve growth factor (NGF)-mediated neuronal differentiation. Gal-3 expression, activation of the MAPK ERK1/2 and neurite outgrowth are induced by NGF and basic fibroblast growth factor (bFGF), but not by ciliary neurotrophic factor (CNTF), epidermal growth factor, insulin or interleukin-6 (IL-6). In addition, in NGF-treated PC12 cells, gal-3 expression, ERK1/2 activation and neurite outgrowth could be specifically inhibited at the level of TrkA, Ras and MAPK-kinase, whereas expression of an oncogenic form of Ras leads to gal-3 expression and neurite outgrowth in the absence of growth factors. In NGF-primed PC12 cells, subsequent treatment with CNTF or IL-6 induces ERK1/2 activation and neurite outgrowth, but not gal-3 expression. Treatment of PC12 cells with staurosporine induces gal-3 expression and neurite outgrowth without ERK1/2 activation. NGF- and staurosporine-induced gal-3-expression is also regulated at the transcriptional level. Our data suggest the presence of complex induction mechanisms of gal-3 expression in neuronally differentiating PC12 cells involving NGF-, but not CNTF- and IL-6-driven (in NGF-primed cells) Ras/MAPK-related signalling pathways. Staurosporine, in contrast, induces gal-3 expression by a Ras/MAPK-independent mechanism.
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PMID:Expression of galectin-3 in neuronally differentiating PC12 cells is regulated both via Ras/MAPK-dependent and -independent signalling pathways. 1462 91

Chagas disease is caused by the parasite Trypanosoma cruzi. The critical initial event is the interaction of the trypomastigote form of the parasite with host receptors. This review highlights recent observations concerning these interactions. Some of the key receptors considered are those for thromboxane, bradykinin, and for the nerve growth factor TrKA. Other important receptors such as galectin-3, thrombospondin, and laminin are also discussed. Investigation into the molecular biology and cell biology of host receptors for T. cruzi may provide novel therapeutic targets.
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PMID:Perspectives on the Trypanosoma cruzi-host cell receptor interactions. 1928 9