N4BP1 — NEDD4 binding protein 1
N4BP1 belongs to a gene co-expression module in 3 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.
N4BP1's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| CD4⁺ T cells | NF-kB feedback TCR/AP1/NFKb pathway | ADTRP, AKAP5, CDIP1, CDKN2A, CLEC7A, INPP1, MAP3K5, PBXIP1 +8 more | View in SCUBA |
| Macrophages | RAB-mediated Trafficking Vesicular traficking | ABI1, ACSL3, ARMC8, CACUL1, CD86, CHST15, CRTC3, CTNNA1 +27 more | View in SCUBA |
| Neutrophils | NF-κB Inflammatory Transcription Inflammatory | BID, C9orf72, DENND5A, ELL2, ETF1, NFE2L2, NFKB1, OXSR1 +10 more |
About the gene
| Chromosome | 16: 48538726-48620148 |
|---|---|
| Predicted location | Intracellular |
| Essential gene | No |
| Protein class | Predicted intracellular proteins |
| Molecular function | Hydrolase, Nuclease, RNA-binding |
| Biological process | Immunity, Innate immunity |
Function
Potent suppressor of cytokine production that acts as a regulator of innate immune signaling and inflammation. Acts as a key negative regulator of select cytokine and chemokine responses elicited by TRIF-independent Toll-like receptors (TLRs), thereby limiting inflammatory cytokine responses to minor insults. In response to more threatening pathogens, cleaved by CASP8 downstream of TLR3 or TLR4, leading to its inactivation, thereby allowing production of inflammatory cytokines (By similarity). Acts as a restriction factor against some viruses, such as HIV-1: restricts HIV-1 replication by binding to HIV-1 mRNAs and mediating their degradation via its ribonuclease activity. Also acts as an inhibitor of the E3 ubiquitin-protein ligase ITCH: acts by interacting with the second WW domain of ITCH, leading to compete with ITCH's substrates and impairing ubiquitination of substrates (By similarity)
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.