High impact information on Stx1b2

• Transcript and protein levels of plasma membrane Ca(2+) ATPase 2 (PMCA2), an essential ion pump expressed exclusively in grey matter and involved in Ca(2+) extrusion, synapsin IIa and syntaxin 1B, important regulators of vesicular exocytosis, were dramatically decreased coincident with the onset of clinical symptoms [1].
• Glucose-stimulated insulin release by syntaxin 1A-overexpressing cells was suppressed to about 50% of the level in control cells, whereas insulin release by syntaxin 1B-overexpressing and control cells did not differ [2].
• The results showed that HPC-1 and syntaxin 1B interrupt the pathways of intracellular membrane transport and inhibit the secretion of ECM by amphibian embryonic cells [3].
• Rat HPC-1/syntaxin 1A and syntaxin 1B interrupt intracellular membrane transport and inhibit secretion of the extracellular matrix in embryonic cells of an amphibian [3].
• HPC-1/syntaxin 1A and syntaxin 1B are proteins that have been implicated in the docking and/or fusion of synaptic vesicles to the presynaptic plasma membrane in neural cells [3].

Biological context of Stx1b2

• The expression of syntaxin 1B is modified in the hippocampus after the induction of long-term potentiation (LTP) and during learning [4].
• These results suggest that syntaxin-1 protein changes in amphetamine-sensitized rats may be due to increased syntaxin-1B gene expression within local neurons of the NAcS that may lead to altered exocytosis from these neurons during the expression of sensitized response [5].

Anatomical context of Stx1b2

• Motor endplates and muscle spindles were only immunostained for syntaxin 1B [6].
• This report shows, for the first time, major differences between the distributions of syntaxin 1A and syntaxin 1B isoforms in the rat central nervous system [7].
• Changes in syntaxin-1B mRNA in the nucleus accumbens of amphetamine-sensitized rats [5].
• Syntaxin 1B was also increased in the ventral dentate gyrus at the same time-points [8].
• In addition to these plasticity-induced changes, a transient increase in the messenger RNA encoding syntaxin 1B was observed at 2 h in conditions of high intensity stimulation of the perforant path to increase the level of cellular activation, but this change was not maintained even when high intensity stimulation was sustained for 5 h [8].

Associations of Stx1b2 with chemical compounds

• We show that 5 h after the induction of LTP, there is an increase in the protein levels of syntaxin 1B and, although to a lesser extent, the synapsins I and II, associated with an increase in depolarization-induced release of glutamate within these terminals [9].

Other interactions of Stx1b2

• BoNT/C is a zinc-endopeptidase that cleaves syntaxin 1A at the Lys253-Ala254 and syntaxin 1B at the Lys252-Ala253 peptide bonds, only when they are inserted into a lipid bilayer [10].
• Zif268, Homer and syntaxin 1B genes were studied, and their regulated expression was examined three times after the induction of long-term potentiation [11].
• These results suggest that LTP and spatial training engage a common pathway utilizing an increase in mRNA for raf B, and demonstrate a dissociation between LTP and spatial learning with respect to expression of zif268 and syntaxin 1B [12].

Analytical, diagnostic and therapeutic context of Stx1b2

• In situ hybridization revealed that from the many messenger RNAs that encode proteins involved in regulated exocytosis, only those encoding synapsin I and syntaxin 1B were specifically increased [8].

References