MFHAS1 — Multifunctional ROCO family signaling regulator 1
MFHAS1 belongs to a gene co-expression module in 2 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.
MFHAS1's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| CD4⁺ T cells | Tfh IL21 help B cell help | APBB2, CDYL2, GDF7, HIF1A, IL21, KIAA1671, MYB, PDCD1 +6 more | View in SCUBA |
| Macrophages | Chromatin Remodeling Housekeeping | ADIPOR2, ADNP, AP2A2, APPL2, ATF2, CDK19, CNOT1, CTDSPL2 +14 more | View in SCUBA |
About the gene
| Synonyms | LRRC65, MASL1 |
|---|---|
| Chromosome | 8: 8783354-8893630 |
| Predicted location | Intracellular |
| Essential gene | No |
| Protein class | Disease related genes, Predicted intracellular proteins |
| Molecular function | Signal transduction inhibitor |
| Biological process | Immunity, Inflammatory response, Innate immunity |
Function
Probable GTP-binding protein. Functions in innate immunity and more specifically the inflammatory response as a regulator of the Toll-like receptor TLR2 and TLR4 signaling pathways. Negatively regulates the part of the TLR4 signaling pathway that leads to the activation of the transcription factor AP-1. By retaining the phosphatase complex PP2A into the cytoplasm, prevents the dephosphorylation of the AP-1 subunit JUN which is required for proper activation of the transcription factor. Both inhibits and activates the TLR2-dependent signaling pathway. Positively regulates the TLR2 signaling pathway to activate specifically the downstream p38 and JNK MAP kinases and promote the polarization of macrophages toward the pro-inflammatory M1 phenotype. It may also play a role in the regulation of inflammation induced by high glucose through the PKB/AKT signaling pathway. Also involved in erythrocyte differentiation through activation of the ERK1/ERK2 signaling pathway.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.