SYN1
Reaktivität: Human
WB, ELISA, IHC
Wirt: Kaninchen
Polyclonal
unconjugated
Applikationshinweise
Recommended Dilution: WB: 1:1000 IHC: 1:500 Quality Control: Western blots performed on each lot.
Beschränkungen
Nur für Forschungszwecke einsetzbar
Format
Liquid
Buffer
100 μL in 10 mM HEPES ( pH 7.5), 150 mM NaCl, 100 μg per ml BSA and 50 % glycerol.
Lagerung
-20 °C
Dagyte, Luiten, De Jager, Gabriel, Mocaër, Den Boer, Van der Zee: "Chronic stress and antidepressant agomelatine induce region-specific changes in synapsin I expression in the rat brain." in: Journal of neuroscience research, Vol. 89, Issue 10, pp. 1646-57, (2011) (PubMed).
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Hintergrund
Synapsin I plays a key role in synaptic plasticity in brain (Feng et al., 2002, Nayak et al., 1996). This effect is due in large part to the ability of the synapsins to regulate the availability of synaptic vesicles for release. The role of synapsin in synaptic plasticity and in synaptogensis is regulated by phosphorylation (Jovanovic et al., 2001, Kao et al., 2002). Ser 549 along with Ser 62 and Ser 67 are the sites of synapsin I that are phosphorylated by MAP kinase (Jovanovic et al., 1996). Phosphorylation and subsequent dephosphorylation of this site is thought to play a key role in synaptic vesicle trafficking. Anti-Phospho-Ser549 Synapsin Western blot of rat cortex lysate showing specific immunolabeling of the ~78k synapsin I phosphorylated at Ser549 (Control). The phosphospecificity of this labeling is shown in the second lane (lambda-phosphatase: (-Ptase). The blot is identical to the control except that it was incubated in (-Ptase (1200 units for 30 min) before being exposed to the phospho Ser549 synapsin I antibody. The immunolabeling is completely eliminated by treatment with (-Ptase.