Sequestosome 1 (SQSTM1) Antibody
357.5€ (100 µg)
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935106861
info@markelab.com
name
Sequestosome 1 (SQSTM1) Antibody
category
Primary Antibodies
provider
Abbexa
reference
abx122537
tested applications
ELISA, IHC
Description
Rabbit Polyclonal against the SQSTM1 protein.
Documents del producto
Instrucciones
Data sheet
Product specifications
| Category | Primary Antibodies |
| Immunogen Target | Sequestosome 1 (SQSTM1) |
| Host | Rabbit |
| Reactivity | Human |
| Recommended Dilution | ELISA: 1/20000 - 1/80000, IHC: 1/100 - 1/200. Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Purification | Purified by antigen affinity column chromatography. |
| Size 1 | 100 µg |
| Size 2 | 1 mg |
| Form | Lyophilized |
| Tested Applications | ELISA, IHC |
| Buffer | Prior to lyophilization: 1% BSA and 0.02% NaN3. |
| Availability | Shipped within 7-15 working days. |
| Storage | Store at -20 °C. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| NCBI Accession | NP_003891.1 |
| Alias | SQSTM1, A170, OSIL, PDB3, ZIP3, p60, p62, p62B, FTDALS3, NADGP, DMRV |
| Background | Antibody anti-SQSTM1 |
| Status | RUO |
| Note | Concentration: Lyophilized form: Not applicable. After reconstitution: 1 mg/ml. - |
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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