MABN762
Anti-VSNL1 Antibody, clone 2D11
clone 2D11, from mouse
Synonym(s):
Visinin-like protein 1, VILIP, VLP-1, Hippocalcin-like protein 3, HLP3
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All Photos(2)
About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
mouse
Quality Level
antibody form
purified antibody
antibody product type
primary antibodies
clone
2D11, monoclonal
species reactivity
bovine, rat, mouse, human
technique(s)
immunohistochemistry: suitable
western blot: suitable
isotype
IgG2bκ
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... VSNL1(7447)
General description
The protein VSNL1, Visinin-like protein 1 (VILIP, or VLP-1), or Hippocalcin-like protein 3 (HLP3) and encoded by the gene VSNL1/VISL1, is a calcium sensor protein that regulates calcium signaling pathways in neurons. In the retina VSNL1 regulates the inhibition of rhodopsin phosphorylation. VSNL1 is expressed specifically in the brain (and is particularly strong in the granule cells of the cerebellum), retina and PNS. VSNL1 levels are up regulated in Alzheimer′s disease but the significance is unknown at present. VSNL1 belongs to the recoverin family of neuronal specific proteins. Interestingly, new research seems so argue that VSHL1 can also be expressed by non-neuronal cells such as epidermal cells and may play a role as a tumor suppressor gene in squamous carcinoma cells and skin cancer.
Immunogen
Recombinant protein corresponding to human VSNL1.
Application
Detect VSNL1 using this Anti-VSNL1 Antibody, clone 2D11 validated for use in western blotting & IHC.
Western Blotting Analysis: 0.5 µg/mL from a representative lot detected VSNL1 in 10 µg of human cerebellum, rat brain, and mouse cerebellum tissue lysate.
Immunohistochemistry Analysis: A representative lot detected VSNL1 in rat cerebellar cortex tissue (courtesy from the laboratory of Gerry Shaw).
Immunohistochemistry Analysis: A representative lot detected VSNL1 in rat cerebellar cortex tissue (courtesy from the laboratory of Gerry Shaw).
Quality
Evaluated by Western Blotting in mouse brain tissue lysate.
Western Blotting Analysis: 0.5 µg/mL of this antibody detected VSNL1 in 10 µg of mouse brain tissue lysate.
Western Blotting Analysis: 0.5 µg/mL of this antibody detected VSNL1 in 10 µg of mouse brain tissue lysate.
Target description
~22 kDa observed
Physical form
Format: Purified
Purified mouse monoclonal IgG2bκ in buffer containing PBS with 0.05% sodium azide.
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
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Storage Class Code
10 - Combustible liquids
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Jessica E Baker et al.
Molecular and cellular endocrinology, 530, 111296-111296 (2021-04-30)
Adequate access to fresh or frozen normal adrenal tissue has been a primary limitation to the enhanced characterization of the adrenal zones via RNA sequencing (RNAseq). Herein, we describe the application of targeted RNAseq to formalin-fixed paraffin-embedded (FFPE) normal adrenal
Juilee Rege et al.
Journal of the Endocrine Society, 4(10), bvaa123-bvaa123 (2020-10-10)
Somatic mutations driving aldosterone production have been identified in approximately 90% of aldosterone-producing adenomas (APAs) using an aldosterone synthase (CYP11B2) immunohistochemistry (IHC)-guided DNA sequencing approach. In the present study, using CYP11B2-guided whole-exome sequencing (WES) and targeted amplicon sequencing, we detected
Kazutaka Nanba et al.
Frontiers in endocrinology, 15, 1286297-1286297 (2024-03-20)
Double somatic mutations in CTNNB1 and GNA11/Q have recently been identified in a small subset of aldosterone-producing adenomas (APAs). As a possible pathogenesis of APA due to these mutations, an association with pregnancy, menopause, or puberty has been proposed. However
Vivek Swarup et al.
Nature medicine, 25(1), 152-164 (2018-12-05)
Identifying the mechanisms through which genetic risk causes dementia is an imperative for new therapeutic development. Here, we apply a multistage, systems biology approach to elucidate the disease mechanisms in frontotemporal dementia. We identify two gene coexpression modules that are
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