Synaptic plasticity: one STEP at a time. Export

@article{citeulike:802107, abstract = {Striatal enriched tyrosine phosphatase (STEP) has recently been identified as a crucial player in the regulation of synaptic function. It is restricted to neurons within the CNS and acts by downregulating the activity of MAP kinases, the tyrosine kinase Fyn and NMDA receptors. By modulating these substrates, STEP acts on several parallel pathways that impact upon the progression of synaptic plasticity. Here, we review recent advances that demonstrate the importance of STEP in normal cognitive function, and its possible involvement in cognitive disorders such as Alzheimer's disease.}, address = {AGY Therapeutics Inc., 270 E. Grand Avenue, South San Francisco, CA 94080, USA.}, author = {Braithwaite, S. P. and Paul, S. and Nairn, A. C. and Lombroso, P. J.}, citeulike-article-id = {802107}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.tins.2006.06.007}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/16806510}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=16806510}, comment = {Braithwaite 2006 review STEP = STOP to synaptic plasticity via deP of ERK, Fyn and NR2B * STEP (STriatum Enriched tyrosin Phosphatase, PTPN5) * splice variants: cytosolic 46, membrane bound 61 (ER, PSD), several inactive variants * KIM - kinase-interactin mitif - binding MAPKs (STEP specific) * both in striatum and central amygdala X only 61 in Hipp, Cx, BLA * main effect post-synaptically, but also present pre-synaptically * D1-PKA-pSTEP (inactive)-prolonged pERK * NMDA-Ca-Calcineurin-STEP (active)-ERK dephosphorylation-STOP plasticity * Targets: MAPKs (ERK, p38alpha, JNK), Fyn, NR2B * Fyn - deP on Tyr420 causes inactivation * NR2B - pFyn-pNR2B-membrane-STEP-internalization, also reduce opening probability and time of NMDA * Alzheimer - Abeta-AchR-Ca-Calcineurin-STEP (active)- deP NR2B and deP Fyn - NMDA internalization }, doi = {10.1016/j.tins.2006.06.007}, issn = {0166-2236}, journal = {Trends Neurosci}, keywords = {alzheimer, darpp-32, erk, glutamate, nmda, step}, month = {August}, number = {8}, pages = {452--458}, posted-at = {2009-06-10 11:43:55}, priority = {0}, title = {Synaptic plasticity: one STEP at a time.}, url = {http://dx.doi.org/10.1016/j.tins.2006.06.007}, volume = {29}, year = {2006} }

TY - JOUR ID - citeulike:802107 L3 - citeulike-article-id:802107 N2 - Striatal enriched tyrosine phosphatase (STEP) has recently been identified as a crucial player in the regulation of synaptic function. It is restricted to neurons within the CNS and acts by downregulating the activity of MAP kinases, the tyrosine kinase Fyn and NMDA receptors. By modulating these substrates, STEP acts on several parallel pathways that impact upon the progression of synaptic plasticity. Here, we review recent advances that demonstrate the importance of STEP in normal cognitive function, and its possible involvement in cognitive disorders such as Alzheimer's disease. IS - 8 JF - Trends Neurosci SN - 0166-2236 AD - AGY Therapeutics Inc., 270 E. Grand Avenue, South San Francisco, CA 94080, USA. EP - 458 TI - Synaptic plasticity: one STEP at a time. VL - 29 SP - 452 KW - alzheimer KW - darpp-32 KW - erk KW - glutamate KW - nmda KW - step N1 - Braithwaite 2006 review STEP = STOP to synaptic plasticity via deP of ERK, Fyn and NR2B * STEP (STriatum Enriched tyrosin Phosphatase, PTPN5) * splice variants: cytosolic 46, membrane bound 61 (ER, PSD), several inactive variants * KIM - kinase-interactin mitif - binding MAPKs (STEP specific) * both in striatum and central amygdala X only 61 in Hipp, Cx, BLA * main effect post-synaptically, but also present pre-synaptically * D1-PKA-pSTEP (inactive)-prolonged pERK * NMDA-Ca-Calcineurin-STEP (active)-ERK dephosphorylation-STOP plasticity * Targets: MAPKs (ERK, p38alpha, JNK), Fyn, NR2B * Fyn - deP on Tyr420 causes inactivation * NR2B - pFyn-pNR2B-membrane-STEP-internalization, also reduce opening probability and time of NMDA * Alzheimer - Abeta-AchR-Ca-Calcineurin-STEP (active)- deP NR2B and deP Fyn - NMDA internalization AU - Braithwaite, SP AU - Paul, S AU - Nairn, AC AU - Lombroso, PJ PY - 2006/08// UR - http://dx.doi.org/10.1016/j.tins.2006.06.007 ER -