|1.||Hayashi, Yoshio: 7 articles (02/2008 - 05/2002)|
|2.||Hayashi, Y: 5 articles (06/2013 - 02/2001)|
|3.||Inserte, Javier: 5 articles (08/2010 - 10/2004)|
|4.||Garcia-Dorado, David: 5 articles (08/2010 - 10/2004)|
|5.||Shintani-Ishida, Kaori: 3 articles (08/2012 - 08/2005)|
|6.||Yoshikawa, Yoshiro: 3 articles (08/2010 - 04/2005)|
|7.||Takaki, Miyako: 3 articles (08/2010 - 04/2005)|
|8.||Taniguchi, Shigeki: 3 articles (08/2010 - 04/2005)|
|9.||Witte, Torsten: 3 articles (01/2009 - 03/2004)|
|10.||Shiari, Reza: 3 articles (02/2008 - 09/2005)|
01/01/2009 - "Lowering perfusion flow to 50% during reperfusion cycles or shortening the cycles (12 cycles of 5 s ischemia-reperfusion) resulted in a further delay in pHi recovery (4.1 +/- 0.2 and 3.5 +/- 0.3 min, respectively), attenuated alpha-fodrin proteolysis, improved functional recovery, and reduced LDH release (47 and 38%, respectively, P < 0.001) and infarct size (36 and 32%, respectively, P < 0.001). "
08/01/2012 - "We previously showed that removal of PLN inhibition of SERCA2a with an antibody to (anti-) PLN reduces cytosolic Ca(2+) overload, thereby attenuating the spread of contraction bands and fodrin proteolysis, during reperfusion after cardiac ischemia. "
04/08/2005 - "Ischemia induced fodrin proteolysis in the ischemic core and the peri-infarct zone within 15 min after reperfusion, with proteolysis developing quickly in the ischemic core and more slowly in the peri-infarct zone. "
09/12/2003 - "Fifteen minutes after ischemia, proteolysis of fodrin took place in putamen, parietal cortex and hippocampal CA1. "
04/09/1999 - "Pronounced fodrin breakdown was observed in the cerebral cortex and striatum at 24 h after ischemia. "
01/01/2011 - "We demonstrate that the administration of deferasirox, a tridentate iron chelator, is associated with diminished tissue iron deposition, attenuated activation of caspases, reduced α-fodrin cleavage, improved membrane integrity, decreased TUNEL reactivity, and attenuated cardiac fibrosis. "
01/01/2011 - "These iron-overload-induced alterations in Akt/Bad phosphorylation and Bax/Bcl-2 ratio were coupled with increased activation of the downstream caspase-9 (40/38- and 17-kDa fragments) and apoptosis executioner caspase-3 (19- and 17-kDa fragments), which were accompanied by evidence of elevated cytoskeletal α-fodrin cleavage (150- and 120-kDa fragments), discontinuity of myocardial membrane dystrophin immunoreactivity, increases in the number of terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL)-positive cells (nucleic DNA fragmentation), and cardiac fibrosis. "
|3.||Brain Ischemia (Cerebral Ischemia)
03/01/1999 - "In the present study, we investigated species differences in the susceptibility of fodrin to calpain activation induced by cerebral ischemia in gerbils, rats, and mice. "
04/08/2005 - "In this study, we investigated the spatial distribution and temporal changes of calpain-catalyzed alpha-fodrin proteolysis in focal cerebral ischemia and examined the effects of a calpain inhibitor. "
|4.||Sjogren's Syndrome (Sjogren Syndrome)
10/01/2005 - "Analysis of in vivo role of alpha-fodrin autoantigen in primary Sjogren's syndrome."
04/01/2005 - "Alpha-fodrin, an intracellular organ-specific cytoskeleton protein is a recently identified autoantigen associated with Sicca- and Sjogren's syndrome (SS). "
02/15/2005 - "The mice developed Sjogren's syndrome-like pathologic changes in the exocrine organs, and this was associated with autoimmunity against a ubiquitous protein, alpha-fodrin. "
05/01/2001 - "A cleavage product of alpha-fodrin may be an important organ-specific autoantigen in the pathogenesis of Sjogren's syndrome (SS), but the mechanisms of alpha-fodrin cleavage remain unclear. "
05/01/2001 - "Possible involvement of EBV-mediated alpha-fodrin cleavage for organ-specific autoantigen in Sjogren's syndrome."
10/01/2008 - "The current study was carried out to investigate mechanisms by which embryonic liver fodrin (ELF), a crucial Smad3/4 adaptor, suppresses liver tumor formation. "
12/01/1989 - "Supranormal levels of fodrin at the apex of enterocytes were also observed in Crohn's disease samples and in the normal-appearing enterocytes adjacent to a tumor. "
01/01/2015 - "Tumor suppression of Transforming Growth Factor (TGF-β) signaling pathway requires an adaptor protein, Embryonic Liver Fodrin (ELF). "
03/23/2006 - "We found that embryonic liver fodrin (ELF), a beta-Spectrin originally identified in endodermal stem/progenitor cells committed to foregut lineage, possesses potent antioncogenic activity and is frequently inactivated in GI cancers. "
11/01/1992 - "Different organizational states of fodrin in cultured MDCK cells are induced by treatment with low pH, calmodulin antagonist TFP, and tumor promoter PMA."
|6.||Caspase 3 (Caspase-3)
|8.||Immunoglobulin G (IgG)
|9.||Immunoglobulin A (IgA)
|5.||Induced Heart Arrest (Cardioplegia)