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• W1971036587 abstract "Background Schizophrenia has been described as a disease of the synapse. On the basis of previous studies reporting reductions in the levels and activity of CK2 (also know as casein kinase 2 or II) in the brain of subjects with schizophrenia, we hypothesized that CK2-mediated phosphorylation of the presynaptic protein syntaxin 1 (Stx 1) is deficient in schizophrenia. This in turn could affect the binding of Stx 1 to its protein partners and result in abnormal neurotransmitter release and synaptic transmission. Methods We analyzed post mortem prefrontal cortex samples from 15 schizophrenia cases and matched controls by quantitative immunoblotting. Results In addition to replicating previous findings of reduced CK2 levels, we show that as predicted, the deficit in CK2 correlates with a deficit in phospho-Stx 1. In contrast, we find that these deficits are not present in depression cases. Further, we show that the reduced levels of CK2 and phospho-Stx 1 are not due to treatment with antipsychotic drugs (APDs). In fact, APDs seem to increase both CK2 and phospho-Stx 1, suggesting that their therapeutic action may be associated with the reversal of these deficits. Finally, we show that lower phospho-Stx 1 levels are associated with reduced binding of Stx 1 to SNAP-25 and MUNC18 and decreased SNARE complex formation. Conclusions Our findings constitute the first report of altered phosphorylation of a key component for neurotransmitter release in humans and suggest that regulation of Stx 1 by CK2-mediated phosphorylation could play a role in the pathophysiology of schizophrenia. Schizophrenia has been described as a disease of the synapse. On the basis of previous studies reporting reductions in the levels and activity of CK2 (also know as casein kinase 2 or II) in the brain of subjects with schizophrenia, we hypothesized that CK2-mediated phosphorylation of the presynaptic protein syntaxin 1 (Stx 1) is deficient in schizophrenia. This in turn could affect the binding of Stx 1 to its protein partners and result in abnormal neurotransmitter release and synaptic transmission. We analyzed post mortem prefrontal cortex samples from 15 schizophrenia cases and matched controls by quantitative immunoblotting. In addition to replicating previous findings of reduced CK2 levels, we show that as predicted, the deficit in CK2 correlates with a deficit in phospho-Stx 1. In contrast, we find that these deficits are not present in depression cases. Further, we show that the reduced levels of CK2 and phospho-Stx 1 are not due to treatment with antipsychotic drugs (APDs). In fact, APDs seem to increase both CK2 and phospho-Stx 1, suggesting that their therapeutic action may be associated with the reversal of these deficits. Finally, we show that lower phospho-Stx 1 levels are associated with reduced binding of Stx 1 to SNAP-25 and MUNC18 and decreased SNARE complex formation. Our findings constitute the first report of altered phosphorylation of a key component for neurotransmitter release in humans and suggest that regulation of Stx 1 by CK2-mediated phosphorylation could play a role in the pathophysiology of schizophrenia." @default.
• W1971036587 created "2016-06-24" @default.
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• W1971036587 date "2010-02-01" @default.
• W1971036587 modified "2023-10-16" @default.
• W1971036587 title "Deficits in Syntaxin 1 Phosphorylation in Schizophrenia Prefrontal Cortex" @default.
• W1971036587 cites W1271531431 @default.
• W1971036587 cites W1492615693 @default.
• W1971036587 cites W1555714096 @default.
• W1971036587 cites W1931583840 @default.
• W1971036587 cites W1964347513 @default.
• W1971036587 cites W1969171865 @default.
• W1971036587 cites W1970802518 @default.
• W1971036587 cites W1972977742 @default.
• W1971036587 cites W1979456591 @default.
• W1971036587 cites W1993034746 @default.
• W1971036587 cites W1997576450 @default.
• W1971036587 cites W1998245695 @default.
• W1971036587 cites W2001813194 @default.
• W1971036587 cites W2002095327 @default.
• W1971036587 cites W2003239731 @default.
• W1971036587 cites W2003432553 @default.
• W1971036587 cites W2006897184 @default.
• W1971036587 cites W2006955548 @default.
• W1971036587 cites W2009639277 @default.
• W1971036587 cites W2018333098 @default.
• W1971036587 cites W2019711009 @default.
• W1971036587 cites W2020320000 @default.
• W1971036587 cites W2031212561 @default.
• W1971036587 cites W2032208151 @default.
• W1971036587 cites W2032499353 @default.
• W1971036587 cites W2040866860 @default.
• W1971036587 cites W2041805953 @default.
• W1971036587 cites W2045198784 @default.
• W1971036587 cites W2045878719 @default.
• W1971036587 cites W2047683495 @default.
• W1971036587 cites W2050511573 @default.
• W1971036587 cites W2051420506 @default.
• W1971036587 cites W2055807160 @default.
• W1971036587 cites W2056293200 @default.
• W1971036587 cites W2056650993 @default.
• W1971036587 cites W2060624196 @default.
• W1971036587 cites W2061387029 @default.
• W1971036587 cites W2078267259 @default.
• W1971036587 cites W2078694877 @default.
• W1971036587 cites W2084157128 @default.
• W1971036587 cites W2088142719 @default.
• W1971036587 cites W2092783107 @default.
• W1971036587 cites W2100453242 @default.
• W1971036587 cites W2100606390 @default.
• W1971036587 cites W2102436536 @default.
• W1971036587 cites W2117879536 @default.
• W1971036587 cites W2120893200 @default.
• W1971036587 cites W2121233493 @default.
• W1971036587 cites W2121235255 @default.
• W1971036587 cites W2126843605 @default.
• W1971036587 cites W2132732528 @default.
• W1971036587 cites W2139395239 @default.
• W1971036587 cites W2144598242 @default.
• W1971036587 cites W2146178083 @default.
• W1971036587 cites W2147284990 @default.
• W1971036587 cites W2147905210 @default.
• W1971036587 cites W2151307579 @default.
• W1971036587 cites W2154100802 @default.
• W1971036587 cites W2162106185 @default.
• W1971036587 cites W2168555817 @default.
• W1971036587 cites W2231154620 @default.
• W1971036587 cites W306153470 @default.
• W1971036587 cites W4244686895 @default.
• W1971036587 cites W4252627448 @default.
• W1971036587 cites W44954597 @default.
• W1971036587 doi "https://doi.org/10.1016/j.biopsych.2009.07.029" @default.
• W1971036587 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19748077" @default.
• W1971036587 hasPublicationYear "2010" @default.
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