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MABN762

Sigma-Aldrich

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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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

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).

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.

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
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
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
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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