Transcriptional Repression
Gene co-expression module in Mucosal-associated invariant T cell
| Category | Immune regulation |
|---|---|
| Genes | 16 |
| Annotation certainty | 3 of 5 |
| Annotation consistency | 10 of 16 genes have a known function matching the annotation |
Why this annotation
This module contains several notable immune regulatory genes. CMIP (c-Maf inducing protein) is a signaling adaptor that activates NF-AT and is involved in T cell differentiation/immunosuppression. TNFRSF1B (TNF receptor 2) mediates TNF signaling in T cells and regulatory T cell function. NR3C1 (glucocorticoid receptor) is a major transcriptional regulator of T cell function and anti-inflammatory responses. MXI1 is a MYC antagonist/transcriptional repressor. RCOR1 (CoREST) is a transcriptional corepressor. SP3 is a general transcription factor. RNF168 is an E3 ubiquitin ligase involved in DNA damage response (H2AK13/15 ubiquitination). RNF115 is an E3 ligase with immune regulatory roles. PELI2 is a Pellino E3 ligase in innate immune/NF-κB signaling. RB1CC1 (FIP200) is an autophagy initiator. ANKRD11 is a transcriptional repressor. TENT4B is a non-canonical poly(A) polymerase. TNRC6A is part of the RISC complex. ZFAND6 and PROSER1 and RFTN1 are less characterized. The convergent theme involves transcriptional repression and immune regulation/suppression (CMIP, NR3C1, RCOR1, MXI1, TNFRSF1B, PELI2), suggesting a module related to T cell immune regulation and signal dampening.
Genes
ANKRD11, CMIP, MXI1, NR3C1, PELI2, PROSER1, RB1CC1, RCOR1, RFTN1, RNF115, RNF168, SP3, TENT4B, TNFRSF1B, TNRC6A, ZFAND6
Most correlated modules
- Epigenetic Chromatin Regulation · correlation 0.79
- Nuclear-Cytoplasmic Transport · correlation 0.72
- Chromatin Regulation · correlation 0.68
- SWI/SNF Chromatin Remodeling · correlation 0.65
- Cytoskeletal Migration · correlation 0.59
- Immune Synapse Signaling · correlation 0.59
Module annotations were drafted by a large language model from the module's genes, then reviewed and approved by a domain expert. See sources & licences.