rabbit anti munc13-2 antibody (Synaptic Systems)
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90
Structured Review
Synaptic Systems
rabbit anti munc13-2 antibody
Rabbit Anti Munc13 2 Antibody, supplied by Synaptic Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rabbit+anti+munc13-2+antibody/munc13+1+antibody/pm31129085-77-55-74
Average 90 stars, based on 1 article reviews
Rabbit Anti Munc13 2 Antibody, supplied by Synaptic Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rabbit+anti+munc13-2+antibody/munc13+1+antibody/pm31129085-77-55-74
Average 90 stars, based on 1 article reviews
rabbit anti munc13-2 antibody - by Bioz Stars,
2026-09
90/100 stars
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Related Articles
Immunocytochemistry:Article Title: The loss of β adrenergic receptor mediated release potentiation in a mouse model of fragile X syndrome. Article Snippet: In fragile X syndrome, the absence of Fragile X Mental Retardation Protein (FMRP) is known to alter postsynaptic function, although alterations in presynaptic function also occur.. We found that the potentiation of glutamate release induced by the β adrenergic receptor (βAR) agonist isoproterenol is absent in cerebrocortical nerve terminals (synaptosomes) from mice lacking FMRP (Fmr1 KO), despite the normal cAMP generation.. The glutamate release induced by moderate stimulation of synaptosomes with 5 mM KCl was not potentiated in Fmr1 KO synaptosomes by isoproterenol, nor by stimulating the receptor associated signaling pathway with the adenylyl cyclase activator forskolin or with the Epac activator 8-pCPT. Affinity Purification:Article Title: The loss of β adrenergic receptor mediated release potentiation in a mouse model of fragile X syndrome. Article Snippet: In fragile X syndrome, the absence of Fragile X Mental Retardation Protein (FMRP) is known to alter postsynaptic function, although alterations in presynaptic function also occur.. We found that the potentiation of glutamate release induced by the β adrenergic receptor (βAR) agonist isoproterenol is absent in cerebrocortical nerve terminals (synaptosomes) from mice lacking FMRP (Fmr1 KO), despite the normal cAMP generation.. The glutamate release induced by moderate stimulation of synaptosomes with 5 mM KCl was not potentiated in Fmr1 KO synaptosomes by isoproterenol, nor by stimulating the receptor associated signaling pathway with the adenylyl cyclase activator forskolin or with the Epac activator 8-pCPT. |