Apoptosis is a kind of programmed cell death that is needed in several physiological processes such as for example embryogenesis, cell turn-over and response to pathogens. OMoreover, the BRAG1 mediated synaptic depression, which involves Arf6 activation, is mediated by synaptic trafficking of GluA1 containing AMPA Rs. Together, these results suggest that BRAG1 Arf6 depresses synaptic transmission via regulating Rap2 JNK PP2B signaling. Our results suggest a novel synaptic signaling mechanism whose dysregulation results in Xlinked mental retardation. MAPK pathway cancer Previous studies have examined the signaling and synaptic mechanisms for 2 other X linked mental issues, oligophrenin 1 linked X linked mental retardation and fragile X syndrome. . Loss of function of oligophrenin 1 is believed to be responsible for the cognitive impairment associated with X associated mental retardation, and recent evidence suggests that oligophrenin 1 signals synaptic treatment of GluA2 containing AMPA Rs in a synaptic activity dependent manner. In while NMDA Kiminas dependent LTP is considerably paid down in the knockout animals, FMR1 knockout mice, a mouse model for fragile X syndrome, mGluAdependent LTD is reasonably up regulated by 10 15%. The increased mGluA dependent LTD is mediated by enhanced Arc signaling, which controls p38 MAPK mediated synaptic removal of GluA2 containing AMPA Rs. High mGluR signaling appears Cellular differentiation accountable for several syndromic options that come with vulnerable X, such as the altered ocular dominance plasticity, seizure and passive avoidance. . The trouble in LTP is a result of the selective impairment of signal transduction between Ras and PI3K that abolishes synaptic distribution of GluA1 containing AMPA Rs. This poor LTP is responsible for the impaired active, high level associative learning linked with fragile X, which can be consistent with the finding that synaptic trafficking of GluA1 containing AMPA Rs is vital for experience dependent synaptic plasticity and associative learning. Here, we report that BRAG1 Arf6 regulates the JNKmediated synaptic elimination hepatitis C virus protease inhibitors of GluA1 containing AMPA Rs. . Furthermore, BRAG1 strains related to nonsyndromic X linked mental retardation impair both JNK signaling and synaptic trafficking of GluA1, although not GluA2 containing AMPA Rs. These results hence provide the initial evidence that dysregulation of JNK signaling and synaptic treatment of GluA1 containing AMPA Rs may also cause X linked mental retardation, and provide a fresh mechanistic explanation for how mutations that either inhibit or enhance Arf6 activity may all end in nonsyndromic X linked mental impairment. n the other hand aberrant apoptosis is implicated in a number of neurodegenerative problems including Parkinsons disease, Huntingtons disease and Alzheimers disease in addition to acute injuries such as stroke and spinal cord injury. Therefore, knowing the upstream signaling pathways that regulate apoptosis in neurons is crucial for the development of treatments for these disastrous neurological conditions.