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VSNL1 is a member of the visinin/recoverin subfamily of neuronal calcium sensor proteins.
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Underexpression of VSNL1 is associated with glioblastoma multiforme.
These data indicate that VILIP-1 alone or in combination with other AD CSF biomarkers represent a valuable marker for the early diagnosis of AD, recognition of MCI patients at higher risk to develop dementia, and in differentiating AD from LBD.
These findings suggest a unique role for cerebrospinal fluid Vilip-1 as a biomarker of entorhinal cortex neuron loss in Alzheimer disease
The results suggest that both serum and cerebrospinal fluid levels of VILIP-1 may be one of predictive markers of acute encephalopathy with biphasic seizures.
We show for the first time that the C-terminus of VILIP-1, containing Cys187, might represent a novel redox-sensitive motif and that VILIP-1 dimerization and aggregation are hallmarks of amyotrophic lateral sclerosis
Results show that in the presence of calcium, N-myristoylation significantly increases the kinetic rate of VILIP adsorption to the membrane.
The results showed that the CSF (show CSF2 ELISA Kits) VILIP-1 level had significantly increased in Alzheimer disease patients compared with both normal controls and Lewy body dementia patients.
SNPs upstream of SLC2A9 (show SLC2A9 ELISA Kits) and within VSNL1 showed strongest evidence for association with AD + P when compared with controls.
VSNL1 single-nucleotide polymorphisms and pathological changes in VILIP-1 protein expression, possibly occurring during brain development, may contribute to the morphological and functional deficits observed in schizophrenia.
Patients with high VSNL-1 expression had significantly poorer prognosis than those with low expression in stage III disease
Findings indicate that VILIP-1 is involved in epithelial-mesenchymal transition (EMT (show ITK ELISA Kits)) of squamous cell carcinoma (SCC (show CYP11A1 ELISA Kits)) cells by regulating the transcription factor Snail1 (show SNAI1 ELISA Kits) in a cAMP-dependent manner.
VSNL1 expresses exclusively in atrial cardiomyocytes during embryogenesis.
VILIP-1 overexpression decreases the susceptibility to skin carcinogenesis in experimental mouse cancer models, thus supporting its role as a tumor suppressor gene
Data show that VILIP-1 led to reduced migration of aggressive SCC (show CYP11A1 ELISA Kits) cells depending on cAMP levels.
Vsnl1 marks ureteric bud tips in embryonic kidneys, and its mosaic pattern demonstrates a heterogeneity of cell types that may be critical for normal ureteric branching.
Decreased or absent VILIP-1 expression in SCC (show CYP11A1 ELISA Kits) cell subpopulations may lead to a more advanced malignant phenotype characterized by changes in adhesive ability and increased cell motility, suggestive of a tumor suppressor function
VILIP1 constitutively binds to P2X2 receptors and displays enhanced interactions in an activation- and calcium-dependent manner owing to exposure of its binding segment in P2X2 receptors
This gene is a member of the visinin/recoverin subfamily of neuronal calcium sensor proteins. The encoded protein is strongly expressed in granule cells of the cerebellum where it associates with membranes in a calcium-dependent manner and modulates intracellular signaling pathways of the central nervous system by directly or indirectly regulating the activity of adenylyl cyclase. Alternatively spliced transcript variants have been observed, but their full-length nature has not been determined.
, visinin-like protein 1
, hippocalcin-like protein 3
, neural visinin-like protein 1
, 21 kDa CABP
, neurocalcin alpha