| 2005 |
BAF155 (SMARCC1) and BAF170 (SMARCC2) protein levels dictate the maximum cellular amount of BAF57; exogenous BAF57 triggers proteasome-dependent degradation of endogenous BAF57, and mapped protein-protein interaction domains between BAF57 and BAF155/BAF170 are required for this regulatory process. |
Exogenous expression of wild-type and deletion mutants, proteasome inhibitor assays, domain-mapping co-immunoprecipitation |
Molecular and cellular biology |
Medium |
16199878
|
| 2019 |
SIRT6 mono-ADP-ribosylates BAF170 (SMARCC2), and this modification is required for SIRT6-mediated transcriptional activation of a subset of NRF2-responsive genes (e.g., HO-1) during oxidative stress; SIRT6 recruits BAF170 to the HO-1 enhancer, promotes RNA Pol II recruitment, and mediates formation of an active 10-kb chromatin loop at the HO-1 locus. |
SIRT6 separation-of-function mutants, in vitro mono-ADP-ribosylation assay, ChIP, chromatin conformation capture (3C/loop analysis), siRNA knockdown |
Nucleic acids research |
High |
31216030
|
| 2016 |
Conditional deletion of BAF170 (SMARCC2) in postnatal dentate gyrus depletes the pool of radial glial-like progenitor cells and promotes terminal astrocyte differentiation, resulting in spatial learning and memory deficits in mice. |
Conditional knockout mouse model, Morris water maze behavioral testing, histological analysis of neural progenitor cell populations |
Molecular neurobiology |
Medium |
27392482
|
| 2015 |
Knockdown of Baf170 (Smarcc2) during late-stage reprogramming improves iPSC colony formation efficiency and promotes complete reprogramming of partially reprogrammed cells (pre-iPSCs); Baf170 expression during reprogramming is regulated by Jak/Stat3 activity. |
shRNA-mediated knockdown in mouse reprogramming assay, iPSC colony counting, pre-iPSC reprogramming assay, Jak/Stat3 inhibitor treatment |
Stem cells and development |
Medium |
26121422
|
| 2021 |
SMARCC2 physically binds c-Myc (co-immunoprecipitation) and its overexpression downregulates c-Myc expression, leading to reduced N-cadherin, vimentin, Snail, and β-catenin levels and elevated T-cadherin, thereby inhibiting EMT, cell migration, and invasion in glioma cells. |
Co-immunoprecipitation, siRNA knockdown, adenoviral overexpression, wound-healing assay, Transwell invasion assay, Western blotting |
Molecular medicine reports |
Low |
34080022
|
| 2022 |
SMARCC2 negatively regulates DKK1 transcription by closing DKK1 promoter chromatin accessibility, thereby preventing binding of the transcription factor EGR1 and inhibiting PI3K-AKT signaling to suppress glioblastoma proliferation; the SWIRM domain of SMARCC2 plays a more important role than the SANT domain in this chromatin remodeling function. |
SMARCC2 knockout and overexpression, ATAC-seq/chromatin accessibility assays, ChIP for EGR1 binding, siRNA knockdown of DKK1, Western blotting for PI3K-AKT pathway, domain deletion analysis, in vivo intracranial xenograft |
Cell death & disease |
Medium |
36418306
|
| 2023 |
FBXO28 (an E3 ubiquitin ligase) targets SMARCC2 for ubiquitination and proteasomal degradation; FBXO28-mediated degradation of SMARCC2 promotes pancreatic cancer cell proliferation, invasion, and metastasis, and overexpression of SMARCC2 reverses the pro-tumorigenic effects of FBXO28. |
Immunoprecipitation-mass spectrometry to identify SMARCC2 as FBXO28 substrate, co-immunoprecipitation, ubiquitination assays, rescue experiments with SMARCC2 overexpression, in vitro and in vivo functional assays |
Aging |
Medium |
37348029
|
| 2024 |
TRIM37 E3 ubiquitin ligase mediates ubiquitin-proteasome-dependent degradation of SMARCC2, and this degradation activates Wnt signaling, promoting sunitinib resistance in renal cell carcinoma cells. |
Co-immunoprecipitation to identify TRIM37-SMARCC2 interaction, western blot for SMARCC2 protein levels upon TRIM37 manipulation, functional assays (colony formation, sphere formation, drug sensitivity) |
Cell death discovery |
Low |
39349442
|
| 2024 |
SMARCC2 silencing in breast cancer suppresses tumorigenesis and cancer stem cell features by reducing chromatin accessibility at enhancers of key oncogenic genes including PIK3CB, thereby downregulating the Ras-PI3K signaling pathway. |
SMARCC2 siRNA/shRNA knockdown, RNA-seq, ATAC-seq for chromatin accessibility, ChIP analysis, cell proliferation and mammosphere assays, xenograft model |
Biochemical and biophysical research communications |
Medium |
38852505
|
| 2025 |
SMARCC2 (BAF170) physically binds HDAC2; Smarcc2 deficiency leads to reduced global histone acetylation and decreased H3K9ac at promoters of synaptic genes (Slc1a3/EAAT1, Slc6a1/GAT1, Slc32a1/VGAT), impairs GABAergic and glutamatergic synaptic currents in PFC pyramidal neurons, and causes working memory deficits; HDAC inhibition with romidepsin restores histone acetylation and working memory. |
Co-immunoprecipitation (SMARCC2-HDAC2 binding), ChIP-seq for SMARCC2 genome-wide binding, RNA-seq, ChIP for H3K9ac at synaptic gene promoters, electrophysiological recordings (GABAergic/glutamatergic currents), behavioral tests, romidepsin pharmacological rescue |
bioRxivpreprint |
Medium |
40492195
|
| 2018 |
Pathogenic variants in SMARCC2 SANT and SWIRM domains (DNA-interacting domains) are associated with more severe neurodevelopmental phenotypes, indicating these domains are functionally critical for SMARCC2's role in the BAF complex during corticogenesis. |
Whole-exome sequencing of 15 affected individuals, genotype-phenotype correlation, domain mapping |
American journal of human genetics |
Low |
30580808
|
| 2023 |
N-terminal missense variants in SMARCC2 decrease protein expression to levels similar to likely gene-disrupting variants, as demonstrated by in vitro testing; non-truncating variants cluster in functional domains and disrupt BAF subunit interactions as assessed by co-immunoprecipitation and proximity-ligation assays. |
In vitro protein expression assays, 3D protein modeling, co-immunoprecipitation, proximity-ligation assays |
Genetics in medicine |
Medium |
37551667
|