Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.28 (chloramphenicol acetyltransferase)
 5,100 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hippocalcin is an EF-hand [Persechini A. et al. (1989) Trends Neurosci. 12, 462-467] Ca2+ binding protein encoded by a neuron-specific gene. A detailed atlas of hippocalcin messenger RNA expression in the adult rat brain was complied using in situ hybridization. Highest levels of messenger RNA are found in the hippocampus, where messenger RNA is localized in proximal dendrites of CA pyramidal cells. Expression is also seen in other brain regions, including the neocortex, caudate-putamen, taenia tecti, claustrum, olfactory tubercle, anterior olfactory nucleus, and granule cell and glomerular layers of the olfactory bulb. The rat hippocalcin gene spans approximately 9 kb and consists of three exons, separated by introns of 6.7 and 0.25 kb. Sequence analysis of the putative proximal promoter region identified two clusters of multiple E-box sites which may regulate the cell-specific expression. Two lacZ fusion constructs carrying 0.9 and 3.4 kb of rat hippocalcin gene upstream region were used to create transgenic mice. With the 3.4 kb construct, transgene expression varied between founder mice, but was always found in the dentate gyrus and CA1-CA4 regions of the hippocampus, thus partly mimicking the expression of the endogenous gene. For the 0.9 kb construct, the levels of lacZ expression were weaker and more variable. Neither construct showed expression in any peripheral tissues examined. To establish an in vitro model of transcriptional regulation, the 3.4 and 0.9 kb 5' upstream regions were fused to a promoterless reporter gene encoding chloramphenicol acetyltransferase and transiently transfected into the hippocalcin-positive NG-108 cells. The 3.4 kb construct was strongly expressed, whilst the 0.9 kb construct was not expressed. In this paper, we describe the detailed expression pattern of the rat hippocalcin gene, the gene structure and its neuron-specific promoter.
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PMID:Characterization of the rat hippocalcin gene: the 5' flanking region directs expression to the hippocampus. 893 44

The role of c-Fos in neurodegeneration or neuroprotection after cerebral ischemia is controversial. To investigate whether early c-Fos induction after ischemia is associated with neuroprotection, rats were subjected to 10 minutes of transient forebrain ischemia and c-Fos expression was examined. Resistant dentate granule cells and neurons in CA2-4 displayed more robust immunoreactivity than vulnerable neurons in the CA1 region of hippocampus during early hours of reperfusion. By 6 hours after reperfusion, c-Fos immunoreactivity was greatly diminished in all areas of the hippocampus. Administration of N-acetyl-O-methyldopamine (NAMDA), a compound previously shown to protect CA1 neurons against ischemia, increased c-Fos immunoreactivity in the CA1 vulnerable region at 6 hours after ischemia and protected SK-N-BE(2)C neurons from oxygen glucose deprivation. Further in vitro study showed that NAMDA potentiated phorbol-12 myristate-13 acetate (PMA)-induced c-Fos expression, AP1 binding activity, and late gene expression determined by chloramphenicol acetyltransferase (CAT) activity from AP1 containing tyrosine hydroxylase promoter-CAT fusion gene in SK-N-BE(2)C neurons. In vivo and in vitro results showed that a neuroprotectant, NAMDA, in concert with another stimulus (for example, ischemia or PMA) up-regulates c-Fos expression and suggested that the early rise of NAMDA-induced c-Fos expression in vulnerable CA1 neurons may account for neuroprotection by means of up-regulating late gene expression for survival.
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PMID:Early c-Fos induction after cerebral ischemia: a possible neuroprotective role. 1133 65