GRIN3B
GRIN3B (Glutamate ionotropic receptor NMDA type subunit 3B) هوَ بروتين يُشَفر بواسطة جين GRIN3B في الإنسان.[1]
المراجع
- "Entrez Gene: GRIN3B glutamate receptor, ionotropic, N-methyl-D-aspartate 3B"، مؤرشف من الأصل في 05 ديسمبر 2010.
قراءة متعمقة
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- "Domain interaction between NMDA receptor subunits and the postsynaptic density protein PSD-95"، Science، 269 (5231): 1737–40، 1995، doi:10.1126/science.7569905، PMID 7569905.
- "Human immunodeficiency virus type 1 tat activates non-N-methyl-D-aspartate excitatory amino acid receptors and causes neurotoxicity"، Ann. Neurol.، 37 (3): 373–80، 1995، doi:10.1002/ana.410370314، PMID 7695237.
- "HIV-1 envelope proteins gp120 and gp160 potentiate NMDA-induced [Ca2+]i increase, alter [Ca2+]i homeostasis and induce neurotoxicity in human embryonic neurons"، Eur. J. Neurosci.، 7 (11): 2285–93، 1996، doi:10.1111/j.1460-9568.1995.tb00649.x، PMID 8563977.
- "Death of cultured human neuroblastoma cells induced by HIV-1 gp120 is prevented by NMDA receptor antagonists and inhibitors of nitric oxide and cyclooxygenase"، Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration، 4 (3): 315–21، 1996، doi:10.1016/1055-8330(95)90021-7، PMID 8581564.
- "Human brain N-methyl-D-aspartate receptors regulating noradrenaline release are positively modulated by HIV-1 coat protein gp120"، AIDS، 10 (5): 463–8، 1996، doi:10.1097/00002030-199605000-00003، PMID 8724036.
- "Direct cytotoxicity of HIV-1 envelope protein gp120 on human NT neurons"، NeuroReport، 7 (5): 1045–9، 1996، doi:10.1097/00001756-199604100-00018، PMID 8804048.
- "HIV-1 gp120-induced neurotoxicity to midbrain dopamine cultures"، Brain Res.، 705 (1–2): 168–76، 1996، doi:10.1016/0006-8993(95)01166-8، PMID 8821747.
- "Prevention of HIV-1 gp120-induced neuronal damage in the central nervous system of transgenic mice by the NMDA receptor antagonist memantine"، Brain Res.، 706 (2): 303–7، 1996، doi:10.1016/0006-8993(95)01197-8، PMID 8822372.
- "The coat protein gp120 of HIV-1 inhibits astrocyte uptake of excitatory amino acids via macrophage arachidonic acid"، Eur. J. Neurosci.، 7 (12): 2502–7، 1996، doi:10.1111/j.1460-9568.1995.tb01048.x، PMID 8845955.
- "Normalization and subtraction: two approaches to facilitate gene discovery"، Genome Res.، 6 (9): 791–806، 1997، doi:10.1101/gr.6.9.791، PMID 8889548.
- "Central nervous system expression of HIV-1 Gp120 activates the hypothalamic-pituitary-adrenal axis: evidence for involvement of NMDA receptors and nitric oxide synthase"، Virology، 226 (2): 362–73، 1997، doi:10.1006/viro.1996.0664، PMID 8955056.
- "HIV-1 Tat induces neuronal death via tumor necrosis factor-alpha and activation of non-N-methyl-D-aspartate receptors by a NFkappaB-independent mechanism"، J. Biol. Chem.، 273 (28): 17852–8، 1998، doi:10.1074/jbc.273.28.17852، PMID 9651389.
- "Tat, a human immunodeficiency virus-1-derived protein, augments excitotoxic hippocampal injury in neonatal rats"، Neuroscience، 88 (2): 585–97، 1999، doi:10.1016/S0306-4522(98)00242-5، PMID 10197777.
- "Glucocorticoid modulation of gp120-induced effects on calcium-dependent degenerative events in primary hippocampal and cortical cultures"، Exp. Neurol.، 158 (1): 164–70، 1999، doi:10.1006/exnr.1999.7080، PMID 10448428.
- "Evidence of HIV type 1 glycoprotein 120 binding to recombinant N-methyl-D-aspartate receptor subunits expressed in a baculovirus system"، AIDS Res. Hum. Retroviruses، 15 (16): 1461–7، 1999، doi:10.1089/088922299309973، PMID 10555109.
- "HIV-1 Tat through phosphorylation of NMDA receptors potentiates glutamate excitotoxicity"، J. Neurochem.، 78 (3): 457–67، 2001، doi:10.1046/j.1471-4159.2001.00396.x، PMID 11483648.
- "HIV-1 Tat causes apoptotic death and calcium homeostasis alterations in rat neurons"، Biochem. Biophys. Res. Commun.، 288 (2): 301–8، 2001، doi:10.1006/bbrc.2001.5743، PMID 11606043.
- "Motoneuron-specific expression of NR3B, a novel NMDA-type glutamate receptor subunit that works in a dominant-negative manner"، J. Neurosci.، 21 (23): RC185، 2002، PMID 11717388.
- بوابة الكيمياء الحيوية
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- بوابة علم الأحياء الخلوي والجزيئي
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