|1.||Cooper, George: 5 articles (12/2010 - 11/2003)|
|2.||Zhang, Qiong: 4 articles (01/2015 - 01/2010)|
|3.||Menick, Donald R: 4 articles (12/2010 - 11/2003)|
|4.||Kuppuswamy, Dhandapani: 4 articles (12/2010 - 11/2003)|
|5.||Cheng, Guangmao: 3 articles (12/2010 - 03/2005)|
|6.||Huang, Yue-sheng: 2 articles (01/2012 - 01/2011)|
|7.||Teng, Miao: 2 articles (01/2012 - 01/2011)|
|8.||Zhang, Jia-ping: 2 articles (01/2012 - 01/2011)|
|9.||Zhang, Dong-xia: 2 articles (01/2012 - 01/2011)|
|10.||Liang, Guang-ping: 2 articles (01/2012 - 01/2010)|
07/20/2001 - "In contrast, the anticonvulsant protection against sound-induced seizures in DBA/2 mice provided by a fully protective dose (20 nmol, i.c.v.) of the mGlu(8) receptor agonist PPG, is not significantly affected by the co-administration of the same Group III antagonists, MSOP, MPPG or MAP4. "
12/01/1998 - "(2S,1'S,2'S,3'R)-2-(2'-carboxy-3'-phenylcyclopropyl)glycine (PCCG-IV), which is a potent mGluR2 antagonist and a group III mGluR agonist at higher doses, increased the PTZ-induced seizure latency (ED50=51 nmol) and this effect was fully reversed by the group III mGluR antagonist, (S)-2-amino-2-methyl-4-phosphonobutanoic acid (MAP4). "
07/20/2001 - "The anticonvulsant protection against sound-induced seizures in DBA/2 mice provided by a fully protective dose (20 nmol, i.c.v.) of the mGlu(4) receptor agonist ACPT-1, is partially reversed by the co-administration of the Group III antagonists, MSOP, (RS)-alpha-methyl-4-phosphonophenylglycine (MPPG) or (S)-2-amino-2-methyl-4-phosphonobutanoic acid (MAP4), in the 20-50 nmol dose range. "
12/03/2010 - "The activity of each was increased persistently during maladaptive hypertrophy, and overexpression of PP2A or PP1 in normal hearts reproduced both the microtubule network phenotype and the dephosphorylation of MAP4 Ser-924 and Ser-1056 seen in hypertrophy. "
07/09/2010 - "The Ser-924 --> Ala MAP4 mutant produced a microtubule phenotype indistinguishable from that seen in pressure overload hypertrophy, such that Ser-924 MAP4 dephosphorylation during pressure overload hypertrophy may be central to this cytoskeletal abnormality."
07/09/2010 - "We first isolated MAP4 from normal and pressure overload-hypertrophied feline myocardium; volume-overloaded myocardium, which has an equal degree and duration of hypertrophy but normal functional and cytoskeletal properties, served as a control for any nonspecific growth-related effects. "
12/01/2004 - "Myocyte contractile malfunction characteristic of pressure overload hypertrophy is recapitulated by cardiac-restricted overexpression of MAP4. "
11/01/2003 - "Cardiac transcriptional upregulation of beta1-tubulin rather than the constitutive beta4-tubulin and of microtubule-associated protein (MAP)4 accompanies hypertrophy, with extensive microtubule decoration by MAP4. "
01/01/2014 - "Phosphorylation-dependent mitochondrial translocation of MAP4 is an early step in hypoxia-induced apoptosis in cardiomyocytes."
01/01/2011 - "We thus propose two possible mechanisms triggered by MAP4: (1) stabilization of MT networks, (2) DYNLT1 modulation, which is connected with VDAC1, and inhibition of hypoxia-induced mitochondrial permeabilization."
01/01/2011 - "MAP4 mechanism that stabilizes mitochondrial permeability transition in hypoxia: microtubule enhancement and DYNLT1 interaction with VDAC1."
01/01/2011 - "We demonstrated that increase in the pool of MAP4 could promote the stabilization of MT networks by increasing the synthesis and polymerization of tubulin in hypoxia. "
01/01/2010 - "Our results demonstrate that hypoxia induces microtubule depolymerization and decreased cell viability via the activation of the p38/MAPK signaling pathway and changes the phosphorylation levels of its downstream effectors, MAP4 and Op18."
04/15/1988 - "We also identified in mouse neuroblastoma Neuro 2a cells a MAP of around 200 kDa which is considered to be MAP4 (Parysek, L. "
01/01/1994 - "These techniques have revealed that thin processes extending from monkey kidney cells (TC-7), and those made by human neuroblastoma cells (IMR-32) in response to retinoic acid, are often deficient in MAP4 immunoreactivity. "
03/01/2005 - "We have shown that 1) in severe pressure overload cardiac hypertrophy, there is extensive microtubule-associated protein 4 (MAP4) decoration of a dense microtubule network; and 2) MAP4 microtubule decoration inhibits muscarinic acetylcholine receptor recycling in neuroblastoma cells. "
|3.||methylserine phosphate (MSOP)
|7.||Small Interfering RNA (siRNA)
|8.||p38 Mitogen-Activated Protein Kinases