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10.1016/0898-6568(94)90023-x http://scihub22266oqcxt.onion/10.1016/0898-6568(94)90023-x 7718410!ä!7718410 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Signal 1994 ; 6 (8): 905-14 Nephropedia Template TP {{tp|p=7718410|t=1994. Mechanisms of ATP-induced Ca2+ signaling in osteoclasts |pdf=|usr=}}{{7718410}} gab.com Text Mechanisms of ATP-induced Ca2+ signaling in osteoclasts JO: Cell Signal http://www.kidney.de/pget.php?&tw=1&pmid=7718410 #FOAvip We investigate the mechanisms underlying the intracellular calcium pulse that occurs in response to extracellular adenosine triphosphate (ATP) in osteoclasts. We find that pre-loading of GDP-beta-S abolishes the response in Ca(2+)-free medium, demonstrating an internal release of Ca2+ via a pathway that involves a G protein. GDP-beta-S does not block in normal Ca(2+)-containing medium, suggesting that ATP also induces a Ca2+ influx across the cell membrane. We confirmed this using the Mn2+ quenching technique, which shows significant opening of Ca2+ channels. We find a smaller response to adenosine diphosphate (ADP) and 2-methylthio-ATP (2-MeSATP), but no response to beta, gamma-methylene-ATP (AMP-PCP), adenosine monophosphate (AMP) or uridine triphosphate (UTP). Prior application of AMP and UTP, but not AMP-PCP, blocks the response to ATP. Our results indicate that the receptor is a P2 subtype that is not characteristic of any previously reported P2 receptor or combination of P2 receptors. Twit Text FOAVip Mechanisms of ATP-induced Ca2+ signaling in osteoclasts ????Cell Signal http://www.kidney.de/pget.php?&tw=1&pmid=7718410 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=7718410 #FOAvip English Wikipedia <ref>{{Cite pmid|7718410}}</ref> Mechanisms of ATP-induced Ca2+ signaling in osteoclasts #MMPMID7718410 Yu H; Ferrier J Cell Signal 1994[Nov]; 6 (8): 905-14 PMID7718410show ga We investigate the mechanisms underlying the intracellular calcium pulse that occurs in response to extracellular adenosine triphosphate (ATP) in osteoclasts. We find that pre-loading of GDP-beta-S abolishes the response in Ca(2+)-free medium, demonstrating an internal release of Ca2+ via a pathway that involves a G protein. GDP-beta-S does not block in normal Ca(2+)-containing medium, suggesting that ATP also induces a Ca2+ influx across the cell membrane. We confirmed this using the Mn2+ quenching technique, which shows significant opening of Ca2+ channels. We find a smaller response to adenosine diphosphate (ADP) and 2-methylthio-ATP (2-MeSATP), but no response to beta, gamma-methylene-ATP (AMP-PCP), adenosine monophosphate (AMP) or uridine triphosphate (UTP). Prior application of AMP and UTP, but not AMP-PCP, blocks the response to ATP. Our results indicate that the receptor is a P2 subtype that is not characteristic of any previously reported P2 receptor or combination of P2 receptors. |Adenosine Diphosphate/pharmacology[MESH] |Adenosine Monophosphate/pharmacology[MESH] |Adenosine Triphosphate/analogs & derivatives/*pharmacology[MESH] |Animals[MESH] |Calcium/*physiology[MESH] |Guanosine Diphosphate/analogs & derivatives/pharmacology[MESH] |Magnesium/pharmacology[MESH] |Osteoclasts/*physiology[MESH] |Pertussis Toxin[MESH] |Rabbits[MESH] |Receptors, Purinergic P2/physiology[MESH] |Signal Transduction[MESH] |Thionucleotides/pharmacology[MESH] |Uridine Triphosphate/pharmacology[MESH]Mechanisms of ATP-induced Ca2+ signaling in osteoclasts (epmc).pdf DeepDyve Pubget Overpricing