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Key Documents

AB1761-I

Sigma-Aldrich

Anti-Protein Gene Product 9.5 Antibody

from rabbit, purified by affinity chromatography

Synonym(s):

Ubiquitin carboxyl-terminal hydrolase isozyme L1, UCH-L1, Neuron cytoplasmic protein 9.5, PGP 9.5, PGP9.5, Ubiquitin thioesterase L1

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About This Item

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

biological source

rabbit

Quality Level

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

purified by

affinity chromatography

species reactivity

human, mouse, rat

species reactivity (predicted by homology)

bovine (based on 100% sequence homology), equine (based on 100% sequence homology), porcine (based on 100% sequence homology)

technique(s)

immunocytochemistry: suitable
immunofluorescence: suitable
immunohistochemistry: suitable (paraffin)
western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... UCHL1(7345)

General description

Ubiquitin carboxyl-terminal hydrolase isozyme L1 (UniProt: P09936; also known as EC: 3.4.19.12, UCH-L1, Neuron cytoplasmic protein 9.5, PGP 9.5, PGP9.5, Ubiquitin thioesterase L1) is encoded by the UCHL1 gene (Gene ID: 7345) in human. UCH-L1 is a member of the peptidase C12 family that can exist as a monomer or homodimer. It is expressed in neurons and cells of the diffuse neuroendocrine system and their tumors and is detected in neuronal cell bodies and processes throughout the neocortex. It displays a weak expression in ovary. About 30% of total UCH-L1 is reported to be associated with membranes in brain. Its levels are shown to be down-regulated in brains from Parkinson disease and Alzheimer disease patients. UCH-L1 is a thiol protease that recognizes and hydrolyzes a peptide bond at the C-terminal glycine of ubiquitin and is involved both in the processing of ubiquitin precursors and of ubiquitinated proteins. It also binds to free monoubiquitin and may prevent its degradation in lysosomes. The homodimeric form may have ATP-independent ubiquitin ligase activity. Mutations in UCHL1 gene are known to cause Parkinson disease 5, a complex neurodegenerative disorder with manifestations ranging from typical Parkinson disease to dementia with Lewy bodies. Some mutations in this gene are also linked to spastic paraplegia 79, where patients display a form of spastic paraplegia, which is characterized by a slow, gradual, progressive weakness and spasticity of the lower limbs.

Immunogen

KLH-conjugated linear peptide corresponding to human Protein Gene Product 9.5.

Application

Detect PGP9.5 using this rabbit polyclonal antibody, Anti-Protein Gene Product 9.5 Antibody validated for use in western blotting, IHC (Paraffin), Immunofluorescence & ICC.
Immunofluorescence Analysis: A 1:200 dilution from a representative lot detected Gene Product 9.5 in human cerebellum.

Immunohistochemistry Analysis: A 1:1,000 dilution from a representative lot detected Gene Product 9.5 in human cerebellum.

Immunocytochemistry Analysis: A 1:100 dilution from a representative lot detected Gene Product 9.5 in E18 rat cortical cells..

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Research Category
Neuroscience
Research Sub Category
Developmental Neuroscience

Quality

Evaluated by Western Blotting in rat brain, human brain, and mouse brain tissue lysate.

Western Blotting Analysis: 0.1 µg/mL of this antibody detected Protein Gene Product 9.5 (UCH-L1) in rat brain, human brain, and mouse brain tissue lysate

Target description

~24 kDa observed. Uncharacterized band(s) may be observed in some cell lysates.

Linkage

Replaces: AB1761 and AB9724

Physical form

Affinity purified
Purified rabbit polyclonal antibody in buffer containing 0.1 M Tris-Glycine, 0.15 M NaCl, pH7.4 with 0.05% sodium azide.

Storage and Stability

Stable for 1 year at 2-8°C from date of receipt.

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Legal Information

DyLight is a registered trademark of Pierce Biotechnology, Inc.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class Code

12 - Non Combustible Liquids

WGK

WGK 1

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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Jung-Eun Choi et al.
Molecular & cellular proteomics : MCP, 17(9), 1803-1823 (2018-07-01)
Chronic physical restraint stress increases oxidative stress in the brain, and dysregulation of oxidative stress can be one of the causes of major depressive disorder. To understand the underlying mechanisms, we undertook a systematic proteomic analysis of hippocampus in a
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eNeuro, 8(5) (2021-09-29)
Understanding masseter muscle (MM) innervation is critical for the study of cell-specific mechanisms of pain induced by temporomandibular disorder (TMDs) or after facial surgery. Here, we identified trigeminal (TG) sensory neuronal subtypes (MM TG neurons) innervating MM fibers, masseteric fascia
Maximilian I Pinkham et al.
American journal of physiology. Regulatory, integrative and comparative physiology, 312(3), R368-R379 (2017-01-06)
Heart failure is characterized by the loss of sympathetic innervation to the ventricles, contributing to impaired cardiac function and arrhythmogenesis. We hypothesized that renal denervation (RDx) would reverse this loss. Male Wistar rats underwent myocardial infarction (MI) or sham surgery
Chiara Traini et al.
Journal of cellular and molecular medicine, 23(6), 4076-4087 (2019-04-05)
Urothelium and Lamina Propria (LP) are considered an integrate sensory system which is able to control the detrusor activity. Complete supra-sacral spinal cord lesions cause Neurogenic Detrusor Overactivity (NDO) whose main symptoms are urgency and incontinence. NDO therapy at first

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