|1.||Ferens, Bartosz: 2 articles (12/2009 - 07/2009)|
|2.||Zawacka-Pankau, Joanna: 2 articles (12/2009 - 07/2009)|
|3.||Pyne, Nigel J: 1 article (04/2013)|
|4.||Bittman, Robert: 1 article (04/2013)|
|5.||Chan, Edmond: 1 article (04/2013)|
|6.||Pyne, Susan: 1 article (04/2013)|
|7.||Alossaimi, Manal: 1 article (04/2013)|
|8.||Williamson, Leon: 1 article (04/2013)|
|9.||Gorshkova, Irina: 1 article (04/2013)|
|10.||Tonelli, Francesca: 1 article (04/2013)|
|1.||Vascular System Injuries
05/20/2002 - "Because a mutant form of Fhit that is functional in tumor suppression and defective in catalysis binds ApppA well, it was hypothesized that Fhit-substrate complexes are the active, signaling form of Fhit. "
05/20/2002 - "Fhit possesses intrinsic ApppA hydrolase activity though ApppA cleavage is not required for tumor suppression. "
05/12/1998 - "Because the His-96 --> Asn substitution of Fhit, which retards ApppA hydrolase activity by seven orders of magnitude, did not block tumor-suppressor activity in vivo, we determined whether this mutation affected ApppA binding or particular steps in the ApppA catalytic cycle. "
12/01/1997 - "Reintroduction of FHIT coding sequences to cancer cell lines with FHIT deletions suppressed the ability of these cell lines to form tumors in nude mice even when the reintroduced FHIT gene had been mutated to allow ApppA binding but not hydrolysis. "
04/01/2013 - "SKi also promotes the formation of a novel pro-apoptotic molecule called diadenosine 5',5'''-P(1),P(3)-triphosphate (Ap3A), which binds to the tumor suppressor fragile histidine triad protein (FHIT). "
12/15/1985 - "Upon heat-shock from 19 to 37 degrees C, Ap4A, Ap3A, and Ap3G increase up to 2.2, 3, and 3.3 times their initial levels, respectively. "
08/11/1986 - "Changes in intracellular levels of Ap3A and Ap4A in cysts and larvae of Artemia do not correlate with changes in protein synthesis after heat-shock."
06/01/1991 - "Under light regimens, the accumulation of Ap4A and Ap4G is more characteristic of heavy-metal-ion-stressed cells, whereas the accumulation of Ap3A, Ap3G and Ap3Gp2 is the dominant feature of heavy-metal-ion or heat-shock treatment during energy deprivation (i.e. "
12/30/1985 - "Diadenosine tri- and tetraphosphates (respectively, Ap3A and Ap4A) accumulate in prokaryotic and eukaryotic cells under heat shock conditions, suggesting they could trigger the synthesis of heat shock proteins (hsps). "
12/01/1983 - "coli accumulate P1,P4-diadenosine-5'-tetraphosphate (AppppA), P1-(adenosine-5')-P3-(guanosine-3'-diphosphate-5')-triphosphate (ApppGpp), P1-(adenosine-5')-P4-(guanosine-5')-tetraphosphate (AppppG), P1-(adenosine-5')-P3-(guanosine-5')-triphosphate (ApppG), and P1,P3-diadenosine-5'-triphosphate (ApppA) after heat shock. "
|4.||Myeloid Leukemia (Leukemia, Myelocytic)
08/01/2012 - "Coronary response to diadenosine triphosphate after ischemia-reperfusion in the isolated rat heart."
08/01/2012 - "Both at basal coronary resting tone and after precontraction with 11-dideoxy-1a,9a-epoxymethanoprostaglandin F(2)(α) (U46619), Ap3A produced concentration-dependent vasodilation in the heart, which was attenuated following ischemia-reperfusion. "
08/01/2012 - "Diadenosine triphosphate (Ap3A) is a vasoactive mediator stored in platelet granules that may be released during coronary ischemia-reperfusion. "
08/01/2012 - "These results suggest that Ap3A induces coronary vasodilation, an effect attenuated by ischemia-reperfusion due to the functional impairment of purinergic P2Y receptors and K(ATP) channels, and/or reduced nitric oxide release. "
|1.||Adenosine Diphosphate (ADP)
|3.||diadenosine triphosphate (ApppA)
|4.||fragile histidine triad protein
|5.||Adenosine Triphosphate (ATP)
|6.||Purinergic P2Y Receptors
|7.||15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
|9.||Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF)