Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.2.1.7 (BAL)
1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We previously reported that cross-linking surface immunoglobulin (sIg) leads to induction of the transcription factor CREB in B lymphocytes through phosphorylation at Ser133, despite the lack of an increase in cAMP. Further, cAMP-raising agents fail to induce CREB Ser133 phosphorylation and CRE-dependent gene expression in these cells, which differs sharply from the situation in PC12 rat pheochromocytoma cells where CREB responds to elevation of cAMP through the activity of protein kinase A. In this study, we characterized the signal transduction pathways leading from sIg engagement to CREB activation. By using specific inhibitors for protein kinase C (PKC), Ca2+/calmodulin-dependent protein kinase II (CaM kinase II), and protein kinase A (PKA), we found that anti-Ig-induced CREB Ser133 phosphorylation depends on PKC, but does not require activation of PKA or CaM kinase II. The differential responsiveness of CREB to forskolin in PC12 cells and BAL-17 B cells may relate to the more marked elevation of cAMP in the former as opposed to the latter; however, high concentrations of dbcAMP which should readily enter B cells and artificially increase cAMP levels still failed to induce CREB Ser133 phosphorylation, even in conjunction with a phosphodiesterase inhibitor. Taken together, the cAMP/PKA pathway does not appear to be as active a contributor to CREB phosphorylation in B lymphocytes as in PC12 cells, and does not appear to be involved in sIg-induced, PKC-dependent, CREB activation.
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PMID:Signaling pathways for antigen receptor-mediated induction of transcription factor CREB in B lymphocytes. 862 May 54

A 17 year-old boy was admitted to the hospital because of severe hypertension (200/130 mmHg), headache, irritability, and sweating. Initial biochemical tests suggested pheochromocytoma, being treated with nifedipine, clonidine and propranolol. However, with report of exposure to mercury vapor, twenty-four-hour urine screening and measurement of blood mercury confirmed intoxication. The patient underwent courses of chelation therapy with dimercaprol (BAL) and penicillamine with remission of symptoms and normalization of blood pressure after 2 months. This case has relevance for current practice reflecting similarity between mercury intoxication and hypertension secondary to pheochromocytoma.
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PMID:[Arterial hypertension due to mercury intoxication with clinico-laboratorial syndrome simulating pheochromocytoma]. 873 21

A 17-year-old boy was admitted to hospital because of severe hypertension (200/130 mmHg), headache, irritability, sweating, etc. Initial biochemical tests suggested pheochromocytoma, being treated with nifedipina, clonidina and propranolol. On reporting exposure to mercury vapour, he underwent twenty-four-hour urine screening and measurement of blood mercury which confirmed intoxication. The patient received courses of chelation therapy with dimercaprol (BAL) and penicillamine with remission of symptoms and normalisation of hypertension after 2 months. This case is relevant to current practice regarding similarity between mercury intoxication and hypertension secondary to pheochromocytoma.
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PMID:[Arterial hypertension due to mercury intoxication with clinical and laboratorial syndrome simulating pheochromocytoma]. 1468 74