Rabbit Recombinant Monoclonal Synapsin I antibody - conjugated to PE.
pH: 7.4
Preservative: 0.02% Sodium azide
Constituents: 98% PBS, 1% BSA
| Application | Reactivity | Dilution info | Notes |
|---|---|---|---|
Application Target Binding Affinity | Reactivity Expected | Dilution info - | Notes - |
Application Antibody Labelling | Reactivity Expected | Dilution info - | Notes - |
Neuronal phosphoprotein that coats synaptic vesicles, and binds to the cytoskeleton. Acts as a regulator of synaptic vesicles trafficking, involved in the control of neurotransmitter release at the pre-synaptic terminal (PubMed:21441247, PubMed:23406870). Also involved in the regulation of axon outgrowth and synaptogenesis (By similarity). The complex formed with NOS1 and CAPON proteins is necessary for specific nitric-oxid functions at a presynaptic level (By similarity).
Synapsin-1, Brain protein 4.1, Synapsin I, SYN1
Rabbit Recombinant Monoclonal Synapsin I antibody - conjugated to PE.
pH: 7.4
Preservative: 0.02% Sodium azide
Constituents: 98% PBS, 1% BSA
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
This product is a recombinant monoclonal antibody, which offers several advantages including:
For more information, read more on recombinant antibodies.
This conjugated primary antibody is released using a quantitative quality control method that evaluates binding affinity post-conjugation and efficiency of antibody labeling.
For suitable applications and species reactivity, please refer to the unconjugated version of this clone. This conjugated antibody is eligible for the Abcam trial program.
Synapsin I also known as SYN1 plays an important role in synaptic function. It is a phosphoprotein with a molecular mass of approximately 78 kDa. Synapsin I is expressed mainly in the neurons of the central nervous system (CNS). It binds to synaptic vesicles and actin cytoskeleton which suggests that it functions in modulating neurotransmitter release at the presynaptic terminals. This modulation occurs as synapsin I undergoes phosphorylation which is critical for its activity.
Synapsin I influences synaptic plasticity and is part of the synaptic vesicle trafficking complex. In its dephosphorylated state Synapsin I associates with synaptic vesicles anchoring them to the actin cytoskeleton. Upon phosphorylation Synapsin I changes conformation causing vesicles to mobilize. This activity supports the modulation of neurotransmitter release impacting learning and memory functions.
Synapsin I participates significantly in the neurotransmitter release cycle and synaptic vesicle trafficking pathway. Protein kinase A (PKA) and Ca2+/calmodulin-dependent protein kinase II (CaMKII) regulate its phosphorylation affecting how Synapsin I contributes to vesicle release. The phosphorylation of Synapsin I at sites such as serine 9 enables its interaction with other proteins like actin and spectrin facilitating vesicle movement.
Altered Synapsin I expression associates with neurological conditions like epilepsy and schizophrenia. In epilepsy dysregulation of Synapsin I phosphorylation processes can result in imbalanced neurotransmitter release potentially leading to seizures. Its connection to schizophrenia involves changes in synaptic plasticity which neurotransmitter systems such as dopamine and related proteins like alpha-synuclein also influence. Understanding these interactions can aid in developing therapeutic strategies.
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This species and application combination has not been tested, but we predict it will work based on strong homology. However, this combination is not covered by our product promise.
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