Hippocalcin-Like 1 Human Recombinant
Sterile filtered colorless solution.
Visinin-Like Protein-1 Human Recombinant
Visinin-Like Protein-1 Human Recombinant, His Tag
Visinin-like proteins (VSNLs) are a subfamily of neuronal calcium sensor (NCS) proteins. These proteins are homologous to visinin, a protein originally identified in the retina. The VSNL subfamily includes VILIP-1 (the founder protein), VILIP-2, VILIP-3, hippocalcin, and neurocalcin δ . These proteins are characterized by their ability to bind calcium ions and play crucial roles in calcium signaling pathways.
Key Biological Properties: VSNLs are calcium-binding proteins that undergo a calcium-myristoyl switch mechanism, allowing them to translocate to cellular membranes in response to calcium binding . They have distinct calcium affinities and membrane-binding kinetics.
Expression Patterns and Tissue Distribution: VSNLs are predominantly expressed in the brain, with restricted expression patterns in various subsets of neurons . For example, VILIP-1 is strongly expressed in granule cells of the cerebellum . Additionally, VILIP-1 has been detected in peripheral organs such as the heart, liver, lung, and testis .
Primary Biological Functions: VSNLs modulate intracellular signaling pathways by regulating the activity of adenylyl cyclase and other targets . They play roles in cyclic nucleotide and MAPK signaling, gene expression, and membrane trafficking .
Role in Immune Responses and Pathogen Recognition: While the primary focus of VSNLs is on neuronal functions, emerging research suggests potential roles in immune responses and pathogen recognition, although this area requires further investigation .
Mechanisms with Other Molecules and Cells: VSNLs interact with various intracellular targets after calcium binding. They modulate cellular signal transduction pathways, including cyclic nucleotide and MAPK signaling .
Binding Partners and Downstream Signaling Cascades: VSNLs interact with components of membrane trafficking complexes, affecting the trafficking of receptors and ion channels such as glutamate receptors and nicotinic acetylcholine receptors . These interactions influence neuronal signaling and differentiation.
Regulatory Mechanisms Controlling Expression and Activity: The expression and activity of VSNLs are regulated at multiple levels, including transcriptional regulation and post-translational modifications . For instance, VILIP-1 expression is down-regulated in Alzheimer’s disease, correlating with the presence of neurofibrillary tangles and amyloid plaques .
Transcriptional Regulation and Post-Translational Modifications: Specific transcription factors and signaling pathways regulate the transcription of VSNL genes. Post-translational modifications, such as phosphorylation, also play a role in modulating their activity .
Biomedical Research: VSNLs are valuable tools in studying calcium signaling and neuronal function. They are used to investigate the mechanisms underlying neurodegenerative diseases and other neurological disorders .
Diagnostic Tools: VILIP-1 has emerged as a potential biomarker for neuronal injury and neurodegenerative diseases such as Alzheimer’s disease . Elevated levels of VILIP-1 in cerebrospinal fluid and serum have been associated with cognitive decline and disease progression .
Therapeutic Strategies: Targeting VSNLs and their signaling pathways holds promise for developing therapeutic strategies for neurodegenerative diseases and other conditions involving calcium dysregulation .
Role Throughout the Life Cycle: VSNLs play crucial roles in neuronal development, differentiation, and function. They are involved in processes such as synaptic plasticity, memory formation, and neuroprotection . Dysregulation of VSNLs has been implicated in aging and age-related diseases, including Alzheimer’s disease .