| 2002 |
TRAP25 (MED30) was identified as a previously uncharacterized integral subunit of the human TRAP/Mediator complex that is metazoan-specific. Antibody-mediated immunodepletion of TRAP25 quantitatively removed essentially all TRAP/Mediator components from HeLa nuclear extract without affecting RNA polymerase II or general transcription factors, demonstrating MED30 is required for both basal and activator-dependent transcription. Adding back purified TRAP/Mediator restored both activities, and simultaneous depletion of TRAP/Mediator and TFIID required addition of both TBP/TAFIIs and TRAP/Mediator for rescue, establishing that TAFIIs and Mediator are jointly required for transcription. |
Antibody immunodepletion of HeLa nuclear extract, reconstitution with purified TRAP/Mediator, in vitro transcription assay |
Molecular and cellular biology |
High |
11909976
|
| 2021 |
Cryo-EM structure of the human Mediator-RNA polymerase II pre-initiation complex revealed that metazoan subunits MED27-MED30 associate with exposed regions in MED14 and MED17 to form the proximal part of the Mediator tail module, which binds transcriptional activators. MED30 thus structurally anchors the tail module to the Mediator core. |
Cryo-electron microscopy of reconstituted 50-subunit human Mediator-PIC complex |
Nature |
High |
33902108
|
| 2021 |
Cardiomyocyte-specific deletion of MED30 (constitutive or inducible) in mice caused rapid cardiac defects and lethality. Critically, ablation of MED30 destabilized the majority of Mediator core subunits (head, middle, tail modules) while the kinase module was preserved, demonstrating MED30 is essential for the structural stability of the overall Mediator complex in vivo. RNAseq identified cardiac transcriptional networks controlled by MED30-dependent Mediator. |
Conditional knockout mouse models (constitutive and inducible cardiomyocyte-specific Cre), western blot quantification of Mediator subunit levels, RNAseq |
PLoS genetics |
High |
34506481
|
| 2011 |
A hypomorphic missense mutation in Med30 in mice caused progressive mitochondrial cardiomyopathy with lethality after weaning. Expression profiling revealed pleiotropic downregulation of cardiac genes required for oxidative phosphorylation and mitochondrial integrity, establishing a mechanistic connection between MED30-dependent Mediator function and induction of the metabolic program for oxidative phosphorylation and fatty acid oxidation. |
ENU-generated hypomorphic mouse missense mutation, expression profiling, dietary intervention (ketogenic diet rescue) |
Proceedings of the National Academy of Sciences of the United States of America |
High |
22106289
|
| 2024 |
MED30 overexpression/amplification (co-amplified with MYC in cancers) recruits additional Mediator components and redirects MYC binding to a novel subset of genomic regulatory sites, alters epigenetic marks, and induces formation of new enhancers driving oncogenic target gene expression. In vivo, MED30 overexpression promotes PDAC tumor growth, and this is attenuated by MYC knockdown, placing MED30 upstream of MYC in this oncogenic transcriptional program. |
Transcriptional profiling of MYC/MED30 single and double overexpression, ChIP-seq for Mediator components and MYC binding sites, epigenetic mark profiling, in vivo xenograft models with MYC knockdown rescue |
Research squarepreprint |
Medium |
38766212
|
| 2014 |
siRNA-mediated knockdown of MED30 in HIV-1-infected cells significantly impaired viral replication at a post-integration step, specifically affecting the formation of unspliced viral transcripts, and compromised HIV transcription induced by Tat. MED30 knockdown thus reduces HIV-1 transcription at the level of transcript elongation/splicing. |
siRNA knockdown in HIV-1-infected cells, RT-PCR for early and unspliced viral transcripts, Tat-induced transcription assay |
The Journal of biological chemistry |
Medium |
25100719
|
| 2015 |
MED30 overexpression in gastric cancer cells increased proliferation, migration, and invasion, whereas MED30 knockdown inhibited these effects and significantly reduced tumorigenicity in SCID mice. MED30 also promoted expression of epithelial-mesenchymal transition (EMT)-related genes. |
Overexpression and siRNA knockdown in gastric cancer cell lines, proliferation/migration/invasion assays, SCID mouse tumorigenicity assay, EMT gene expression analysis |
PloS one |
Medium |
26110885
|
| 2019 |
In Drosophila cells, the MED30 subunit of the Mediator complex directs Nipped-B and Rad21 (cohesin subunit) to gene promoters, as shown by genome-wide ChIP-seq. This is distinct from the role of SA and Fs(1)h (BRD4) in directing cohesin to enhancers, indicating that MED30 mediates promoter-specific cohesin recruitment. |
Genome-wide ChIP-seq in Drosophila cells for cohesin subunits (Nipped-B, SA, SMC1, Rad21) combined with MED30 perturbation data |
Genome research |
Medium |
30796039
|
| 2022 |
CRISPR-Cas9-mediated deletion of enhancer regions at the SLC30A8 locus reduced MED30 expression, and subsequent loss of MED30 markedly reduced pancreatic beta cell viability, establishing a required role for MED30 in beta cell survival. |
CRISPR-Cas9 enhancer deletion in human EndoC-βH3 cells, cell viability assays after MED30 loss |
FASEB journal |
Medium |
38661000
|
| 2020 |
MED30 is induced in glioblastoma cells under hypoxia and nutrient deprivation in a HIF1α- and p53-dependent manner, with functional HREs and a p53 binding site identified in the MED30 promoter. MED30 overexpression promoted cell proliferation while reducing migration in GBM cell lines; knockdown had the opposite effects and conferred resistance to temozolomide. MED30 also modulated p53 protein levels in vitro. |
Promoter analysis (HRE and p53 binding site identification), overexpression and siRNA knockdown in GBM cell lines, proliferation and migration assays, temozolomide sensitivity assays, p53 western blot |
Cellular and molecular neurobiology |
Medium |
32705436
|
| 2024 |
Overexpression of MED30 failed to restore protein levels of Mediator subunits in MED27-deficient cardiomyocytes, demonstrating that MED27's role in maintaining Mediator complex integrity is independent of MED30 (negative epistasis result). |
MED30 overexpression in MED27 cardiomyocyte-specific knockout mouse hearts, western blot for Mediator subunit levels |
Life sciences |
Medium |
39209248
|
| 2017 |
siRNA-mediated knockdown of MED30 in clear cell renal cell carcinoma cell lines (ACHN and A-498) significantly decreased proliferation, migration, and invasion. |
siRNA knockdown in ccRCC cell lines, proliferation, migration, and invasion assays |
Annals of diagnostic pathology |
Low |
29661722
|
| 2017 |
siRNA-mediated knockdown of MED30 in bladder cancer cell lines (T24 and TCCSUP) reduced proliferation, migration, and invasion despite higher MED30 expression being associated with better patient survival at the clinical level. |
siRNA knockdown in bladder cancer cell lines, proliferation, migration, and invasion assays |
Anticancer research |
Low |
29187445
|
| 2026 |
Genome-wide CRISPR loss-of-function screen in multiple myeloma cells identified MED30 (Mediator complex subunit) as an activator of endogenous MYC expression; functional validation confirmed that MED30 loss significantly reduced MYC protein levels. |
Genome-wide CRISPR-Cas9 screen with GFP-tagged endogenous MYC reporter, sgRNA validation in MM cell lines |
Scientific reports |
Low |
41965876
|