Anti-phospho-SYT1 (pSer309) antibody produced in rabbit
affinity isolated antibody
Synonym(s):
Anti-DKFZp781D2042 antibody produced in rabbit, Anti-P65 antibody produced in rabbit, Anti-SVP65 antibody produced in rabbit, Anti-SYT antibody produced in rabbit, Anti-synaptotagmin I antibody produced in rabbit
Peptide sequence around phosphorylation site of serine 309 (G-L-S(p)-D-P), according to the protein SYT1.
Features and Benefits
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Target description
The synaptotagmins are integral membrane proteins of synaptic vesicles thought to serve as Ca(2+) sensors in the process of vesicular trafficking and exocytosis. Calcium binding to synaptotagmin I participates in triggering neurotransmitter release at the synapse.
Physical form
Solution in phosphate-buffered saline containing 0.02% sodium azide and 50% glycerol
European journal of pharmacology, 857, 172449-172449 (2019-06-18)
Endoplasmic reticulum stress (ERS)-induced cardiomyocyte apoptosis plays an important role in the pathological process following myocardial infarction (MI). Macrophages that express microRNA-155 (miR-155) mediate cardiac inflammation, fibrosis, and hypertrophy. Therefore, we investigated if miR-155 regulates ERS-induced cardiomyocyte apoptosis after MI
European journal of pharmacology, 851, 122-132 (2019-02-06)
Inflammation plays an important role in sympathetic neural remodeling induced by myocardial infarction (MI). MiR-155 is a vital regulator of inflammatory responses, and macrophage-secreted miR-155 promotes cardiac fibrosis and hypertrophy. However, whether miR-155 influences MI-induced sympathetic neural remodeling is not
Hypoxic zones are common features of metastatic tumors. Due to inactivation of the von Hippel-Lindau gene (VHL), renal cell carcinomas (RCC) show constitutive stabilization of the alpha subunit of the hypoxia-inducible factor (HIF). Thus, RCC represents a model of chronic
Journal of immunology (Baltimore, Md. : 1950), 202(10), 2957-2970 (2019-04-07)
MAVS is a critical adaptor required for activating an innate antiviral immune response against viral infection. The activation of MAVS requires modification of the Lys63-linked ubiquitination and formation of prion-like aggregates. However, the molecular mechanisms regulating MAVS activity remain largely
The mechanisms underlying the role of CXCL5 in tumor angiogenesis have not been fully defined. Here, we examined the effect of CXCL5 on tumor angiogenesis in colorectal cancer (CRC). Immunohistochemistry was used to monitor the expression of CXCL5 and CD31
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