TRAF3 Interacting Protein 1 (TRAF3IP1) Antibody
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Description
TRAF3IP1 play an inhibitory role on IL13 signaling by binding to IL13RA1. Involved in suppression of IL13-induced STAT6 phosphorylation, transcriptional activity and DNA-binding. Recruits TRAF3 and DISC1 to the microtubules.
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Product specifications
| Category | Primary Antibodies |
| Immunogen Target | TRAF3 Interacting Protein 1 (TRAF3IP1) |
| Host | Rabbit |
| Reactivity | Human |
| Recommended Dilution | WB: 1/1000. Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Purification | Purified through a protein A column, followed by peptide affinity purification. |
| Size 1 | 80 µl |
| Size 2 | 400 µl |
| Form | Liquid |
| Tested Applications | ELISA, WB |
| Buffer | PBS containing 0.09% sodium azide. |
| Availability | Shipped within 5-10 working days. |
| Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | Q8TDR0 |
| Alias | IFT54, MIPT3,Interleukin-13 receptor alpha 1-binding protein 1,Intraflagellar transport protein 54 homolog, CFAP116, FAP116, IFT54, MIP-T3, SLSN9 |
| Background | Antibody anti-TRAF3IP1 |
| Status | RUO |
Descripción
TRAF3IP1, also known as IFT54, is a signaling adaptor protein that interacts with TRAF3 and participates in immune signaling and intracellular transport processes. It is a critical component of the intraflagellar transport (IFT) machinery, which regulates ciliogenesis and ciliary signaling pathways by mediating the transport of cargo proteins within primary cilia. TRAF3IP1 plays a key role in developmental processes, cell signaling, and tissue homeostasis by facilitating cilia assembly and function. It is expressed in ciliated epithelial tissues, immune cells, and the brain, where it regulates processes such as Hedgehog signaling, immune response, and cytoskeletal organization. Dysregulation or mutations in TRAF3IP1 are associated with ciliopathies, including Joubert syndrome and nephronophthisis, due to defective cilia function and signaling. Knockout studies reveal impaired ciliogenesis, disrupted signaling pathways, and developmental abnormalities, emphasizing its essential role in cilia-mediated signaling and cellular organization.
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