Sequestosome 1 (SQSTM1) Antibody (FITC)

Este producto es parte de SQSTM1 - Sequestosome-1
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169€ (20 µg)

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935106861
info@markelab.com
name
Sequestosome 1 (SQSTM1) Antibody (FITC)
category
Primary Antibodies
provider
Abbexa
reference
abx313343

Description

SQSTM1 Antibody (FITC) is a Rabbit Polyclonal against SQSTM1 conjugated to FITC.

Documents del producto

Instrucciones
Data sheet
Descargar

Product specifications

Category
Primary Antibodies
Immunogen Target
Sequestosome 1 (SQSTM1)
Host
Rabbit
Reactivity
Human
Recommended Dilution
Optimal dilutions/concentrations should be determined by the end user.
Clonality
Polyclonal
Conjugation
FITC
Isotype
IgG
Purity
> 95%
Purification
Purified by Protein G.
Size 1
20 µg
Size 2
50 µg
Size 3
100 µg
Size 4
200 µg
Size 5
1 mg
Form
Liquid
Buffer
0.01 M PBS, pH 7.4, 0.03% Proclin-300 and 50% Glycerol.
Availability
Shipped within 5-10 working days.
Storage
Aliquot and store at -20°C. Avoid exposure to light. Avoid repeated freeze/thaw cycles.
Dry Ice
No
UniProt ID
Q13501
Gene ID
8878
NCBI Accession
NP_001135770.1, NM_001142298.1, NP_001135771.1, NM_001142299.1, NP_003891.1, NM_003900.4
OMIM
167250
Alias
SQSTM1, A170, OSIL, PDB3, ZIP3, p60, p62, p62B, FTDALS3, NADGP, DMRV
Background
Antibody anti-SQSTM1
Status
RUO

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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