Sequestosome 1 (SQSTM1) Antibody

Este producto es parte de SQSTM1 - Sequestosome-1
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364€ (100 µg)

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935106861
info@markelab.com
name
Sequestosome 1 (SQSTM1) Antibody
category
Primary Antibodies
provider
Abbexa
reference
abx239900
tested applications
ELISA, WB, IHC, IF/ICC

Description

Sequestosome-1 (P62/SQSTM1) Antibody is a Mouse Monoclonal antibody for the detection of P62/SQSTM1.

Documents del producto

Instrucciones
Data sheet
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Product specifications

CategoryPrimary Antibodies
Immunogen TargetSequestosome 1 (SQSTM1)
HostMouse
ReactivityHuman
Recommended DilutionWB: 1/1000 - 1/4000, IHC: 1/50 - 1/500, IF/ICC: 1/20 - 1/200. Optimal dilutions/concentrations should be determined by the end user.
ClonalityMonoclonal
ConjugationUnconjugated
IsotypeIgG2a
Purity≥ 95% (SDS-PAGE)
PurificationPurified by Protein A and Protein G affinity chromatography.
Size 1100 µg
FormLiquid
Tested ApplicationsELISA, WB, IHC, IF/ICC
BufferPBS, pH 7.3, with 0.02% sodium azide and 50% glycerol.
AvailabilityShipped within 5-12 working days.
StorageAliquot and store at -20°C. Avoid repeated freeze/thaw cycles.
Dry IceNo
UniProt IDQ13501
Gene ID8878
OMIM167250
AliasSQSTM1, A170, OSIL, PDB3, ZIP3, p60, p62, p62B, FTDALS3, NADGP, DMRV
BackgroundAntibody anti-SQSTM1
StatusRUO
NoteConcentration: 2 mg/ml - Validity: 12 months.

Descripción

SQSTM1, also known as p62, is an adaptor protein involved in selective autophagy, protein degradation, and cellular stress responses. It acts as a scaffold protein that interacts with ubiquitinated proteins and autophagy-related proteins like LC3, facilitating the delivery of misfolded or damaged proteins to the autophagosome for degradation. SQSTM1 also functions in signaling pathways such as NF-κB activation, oxidative stress responses, and mTOR signaling, where it regulates inflammation, apoptosis, and metabolism. It is highly expressed in various tissues and is essential for maintaining protein homeostasis under stress conditions. Dysregulation or mutations in SQSTM1 are associated with neurodegenerative diseases like ALS and Parkinson’s disease, Paget's disease of bone, and cancer due to impaired autophagy and accumulation of protein aggregates. Knockout studies reveal defects in autophagic flux, increased oxidative stress, and disrupted cellular homeostasis, underscoring its central role in protein quality control and cellular stress adaptation.

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