Affinage

BANP

Protein BANP · UniProt Q8N9N5

Length
519 aa
Mass
56.5 kDa
Annotated
2026-06-09
70 papers in source corpus 43 papers cited in narrative 43 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BANP (also known as SMAR1) is a BEN-domain transcription factor that binds unmethylated CGCG/T(C/G)-repeat motifs at CpG-island promoters and matrix/scaffold-attachment regions (MARs), where it organizes chromatin and controls gene expression (PMID:34234345, PMID:10950932, PMID:27671416). Its DNA recognition is methylation-sensitive at the genomic level—DNA methylation of the motif repels binding and restricts occupancy to unmethylated CpG islands—and upon binding BANP opens chromatin, phases nucleosomes, and activates essential metabolic genes (PMID:34234345). Structural work resolved the BEN domain bound to CGCG DNA, showing that oligomerization underlies its selectivity for unmethylated CGCG motifs (PMID:37086783, PMID:39225042). At MAR elements BANP most often acts as a transcriptional repressor by recruiting HDAC1/mSin3A and related corepressor complexes to target promoters, silencing genes including cyclin D1, Slug, β-catenin, STAT3, hTERT, calnexin, PPARγ and the miR-371-373 cluster (PMID:16166625, PMID:25086032, PMID:29765542, PMID:27671416, PMID:34551340, PMID:31422285, PMID:34450266). BANP is also a positive regulator of p53: it directly binds and stabilizes p53 by inhibiting MDM2-mediated degradation, then later forms a p53-MDM2-BANP ternary complex that recruits HDAC1 to deacetylate p53 and switch off the response during stress recovery (PMID:15701641, PMID:19303885, PMID:20075864). Beyond transcription, BANP regulates alternative splicing by recruiting HDAC6 to deacetylate the RNA-binding proteins Sam68 and PTBP1, controlling CD44 and PKM splicing (PMID:26080397, PMID:33863392), and is required for the DNA-damage response and chromosome segregation, regulating direct targets such as wrnip1, cenpt and ncapg (PMID:35942692). BANP protein levels are tightly governed by APC/C-Cdc20- and RBX1-mediated D-box-dependent ubiquitin-proteasomal degradation (PMID:28617439, PMID:29765542, PMID:36810109).

Mechanistic history

Synthesis pass · year-by-year structured walk · 8 steps
  1. 2000 Medium

    Established the protein's biochemical identity as a sequence-specific nuclear matrix/MAR-binding factor, defining its first functional category.

    Evidence EMSA and GST-pulldown competition on the TCRβ MARβ element, with domain homology to SATB1 and Cux/CDP

    PMID:10950932

    Open questions at the time
    • No genome-wide binding map
    • Functional consequence of MAR binding undefined at this stage
  2. 2003 Medium

    Linked BANP/SMAR1 to tumor suppression via p53, raising the question of how it influences the p53 pathway.

    Evidence Co-IP, co-localization, p53/p21 reporter assays, and in vivo B16F1 tumor model

    PMID:12494467

    Open questions at the time
    • Mechanism of p53 activation not resolved
    • Direct vs. indirect interaction unclear
  3. 2005 High

    Defined the canonical repression mechanism — recruitment of SIN3/HDAC1/pocket-Rb to MAR-containing promoters — and the mechanism of p53 stabilization.

    Evidence Co-IP, ChIP and domain mapping on cyclin D1; in vitro PKC phosphorylation, mutagenesis (Ser347) and MDM2-degradation assays for p53

    PMID:15701641 PMID:16166625

    Open questions at the time
    • Whether one corepressor complex serves all targets
    • Phosphorylation-state control of target selection unmapped
  4. 2010 High

    Resolved how BANP sets the apoptotic threshold by toggling p53 acetylation, establishing a stress-dependent molecular switch.

    Evidence ChIP, EMSA, Co-IP and genetic epistasis in p53-null cells on BAX/PUMA; PML-body sequestration upon apoptotic damage

    PMID:19303885 PMID:20075864

    Open questions at the time
    • Signals controlling PML sequestration not fully defined
    • Quantitative threshold setting unmodeled
  5. 2015 High

    Extended BANP function beyond transcription to splicing control through HDAC-mediated deacetylation of RNA-binding proteins.

    Evidence Co-IP, CLIP, fractionation, phospho-site mutagenesis and in vivo metastasis for Sam68/CD44; ERK phosphorylation controlling localization

    PMID:26080397

    Open questions at the time
    • Breadth of splicing targets unknown
    • Generality of HDAC6-deacetylation mechanism across substrates untested at this point
  6. 2017 High

    Identified the degradation machinery controlling BANP abundance, explaining stress- and cell-cycle-coupled regulation of its levels.

    Evidence Co-IP, ubiquitylation assays, D-box mutagenesis and shRNA rescue showing APC/C-Cdc20-mediated K48 polyubiquitylation

    PMID:28617439

    Open questions at the time
    • Other E3 ligases not excluded at this stage
    • Coupling of degradation to specific cell-cycle phases incompletely mapped
  7. 2021 High

    Redefined BANP as a methylation-sensitive CpG-island activator that opens chromatin, unifying earlier MAR-binding observations with genome-scale function.

    Evidence Single-molecule footprinting, interaction proteomics, in vitro methylation-sensitivity and chromatin-opening assays in stem and neuronal cells

    PMID:34234345

    Open questions at the time
    • Reconciliation of activator vs. repressor roles at different loci
    • Determinants of activation vs. repression unresolved
  8. 2024 High

    Provided the structural basis for methylation-sensitive recognition, showing oligomerization drives selection of unmethylated CGCG motifs.

    Evidence X-ray crystallography of the BEN domain with cognate DNA, plus ITC, PBM and oligomerization analysis

    PMID:37086783 PMID:39225042

    Open questions at the time
    • In vitro ITC showed comparable methylated/unmethylated affinity, contrasting with cellular selectivity
    • Full-length protein behavior on chromatin not crystallized

Open questions

Synthesis pass · forward-looking unresolved questions
  • How BANP integrates its dual identity as a CpG-island chromatin-opening activator and an HDAC-recruiting MAR repressor — i.e., what determines activation versus repression at a given locus — remains unresolved.
  • No unified model linking methylation-sensitive binding to opposite transcriptional outcomes
  • Locus-specific cofactor determinants undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 5 GO:0140110 transcription regulator activity 3 GO:0140096 catalytic activity, acting on a protein 2
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 2 GO:0005654 nucleoplasm 1
Pathway
R-HSA-392499 Metabolism of proteins 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-4839726 Chromatin organization 2 R-HSA-73894 DNA Repair 2 R-HSA-8953854 Metabolism of RNA 2 R-HSA-5357801 Programmed Cell Death 1
Partners
CDC20CUX1HDAC1HDAC6MDM2P300RBX1TP53
Complex memberships
HDAC1/mSin3A corepressor complexp53-MDM2-SMAR1 ternary complex

Evidence

Reading pass · 43 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2021 BANP (SMAR1) is the transcription factor that binds the CGCG element (Banp motif) at CpG island promoters in mouse and human genomes, identified by combining single-molecule footprinting with interaction proteomics. BANP binding is repelled by DNA methylation of its motif in vitro and in vivo, restricting binding to unmethylated CGIs. Upon binding, BANP opens chromatin and phases nucleosomes, activating essential metabolic genes in pluripotent stem and neuronal cells. Single-molecule footprinting, interaction proteomics, in vitro DNA-binding assays, in vivo ChIP, chromatin accessibility assays, loss-of-function experiments Nature High 34234345
2023 Crystal structures of the BANP BEN domain in apo form and in complex with CGCG-containing DNA revealed that the BEN domain uses primarily electrostatic interactions to bind DNA with some base-specific interactions with TC motifs. An optimal binding sequence of AAATCTCG was identified by protein binding microarray and confirmed by isothermal titration calorimetry (ITC) and mutagenesis. ITC showed BANP bound unmethylated and methylated DNAs with comparable affinities in this structural context. X-ray crystallography, protein binding microarray, isothermal titration calorimetry, mutagenesis The Journal of biological chemistry High 37086783
2024 Crystal structures of the BANP BEN domain in complex with cognate DNA substrates revealed that oligomerization is required for BANP to select unmethylated CGCG motif-containing DNA substrates, clarifying the mechanism by which BANP functions as a CpG island-binding protein preferring unmethylated CpG motifs. X-ray crystallography, DNA binding assays, oligomerization analysis Nucleic acids research High 39225042
2022 In zebrafish, Banp is required for DNA damage response and chromosome segregation during mitosis. banp mutants show DNA replication stress, tp53-dependent DNA damage responses, and defective chromosome segregation from prometaphase to anaphase. RNA- and ATAC-sequencing identified direct Banp target genes carrying the Banp motif, including the DNA replication fork regulator wrnip1 and chromosome segregation regulators cenpt and ncapg. Zebrafish genetic mutants and morphants, RNA-seq, ATAC-seq, live imaging, loss-of-function with defined phenotypic readouts eLife High 35942692
2000 SMAR1 (BANP) was identified as a novel MAR-binding protein that binds the MARbeta scaffold/matrix-associated region 400 bp upstream of the TCRbeta enhancer. GST-SMAR1 fusion protein binding to MARbeta was competed by excess MAR-containing DNA from the immunoglobulin kappa locus. SMAR1 shares homology with SATB1 and Cux/CDP in the MAR-binding/Cut repeat domain and with the tetramerization domain of Bright. Electrophoretic mobility shift assay (EMSA), GST pulldown, yeast two-hybrid (initial identification), domain homology analysis Genomics Medium 10950932
2000 BANP (BTG3-associated nuclear protein) was identified via yeast two-hybrid screening using BTG3 as bait. The protein was localized to human chromosome 16q24, a region with frequent loss of heterozygosity in tumors. Yeast two-hybrid, chromosomal mapping Gene Low 10940556
2005 SMAR1 represses cyclin D1 gene expression by recruiting a repressor complex containing SIN3, HDAC1, and pocket retinoblastoma proteins to the cyclin D1 promoter MAR, resulting in histone deacetylation spreading at least 5 kb upstream. The interaction is mediated by the SMAR1(160–350) domain. Co-immunoprecipitation, ChIP, reporter assay, siRNA knockdown, domain mapping Molecular and cellular biology High 16166625
2003 SMAR1 physically interacts and colocalizes with p53, and the shorter isoform SMAR1(S) activates p53-mediated reporter gene expression and its downstream effector p21. Overexpression of SMAR1(S) in B16F1 melanoma cells delays tumor growth in C57BL/6 mice and causes G2/M phase retardation. Co-immunoprecipitation, co-localization (immunofluorescence), reporter assay, in vivo tumor model, cell cycle analysis International journal of cancer Medium 12494467
2005 The arginine-serine (RS)-rich domain of SMAR1 is phosphorylated by protein kinase C family proteins and is responsible for p53 interaction, activation, and stabilization within the nucleus. SMAR1-mediated stabilization of p53 occurs by inhibiting Mdm2-mediated degradation of p53. In vitro phosphorylation assays with point-mutated peptides identified serine 347 as indispensable for activity. Domain deletion/mutation, in vitro phosphorylation assay, Co-IP, siRNA knockdown, transgenic mice The Journal of biological chemistry High 15701641
2009 SMAR1 interacts with MDM2 and the Ser15-phosphorylated form of p53, forming a ternary complex in the post-stress recovery phase. This triple complex recruits HDAC1 to deacetylate p53, which then binds poorly to the p21 promoter, switching off the p53 response. siRNA knockdown of SMAR1 led to prolonged cell-cycle arrest in the post-stress recovery phase. Co-immunoprecipitation, ChIP, siRNA knockdown, reporter assay Journal of molecular biology Medium 19303885
2010 SMAR1 selectively represses BAX and PUMA by binding to an identical MAR element in their promoters and inducing HDAC1-mediated p53 deacetylation, generating an anti-apoptotic response and cell cycle arrest upon mild DNA damage. Upon apoptotic DNA damage, PML nuclear bodies sequester SMAR1, releasing BAX and PUMA repression. SMAR1 knockdown induces apoptosis that is abrogated in the absence of p53. ChIP, EMSA, siRNA knockdown, Co-IP, immunofluorescence, epistasis with p53 null cells The EMBO journal High 20075864
2004 SMAR1 and Cux/CDP modulate chromatin structure at MARbeta by DNaseI hypersensitivity, independently repress Ebeta-dependent reporter gene expression, and physically interact with each other. The repressor activity of SMAR1 is enhanced by Cux/CDP; they colocalize in the perinuclear region through a SMAR1 repression domain that is separate from the MAR-binding domain and contains a nuclear localization signal and RS-rich domain. DNaseI hypersensitivity assay, reporter assay, Co-immunoprecipitation, immunofluorescence co-localization, domain mapping Nucleic acids research Medium 15371550
2004 SMAR1-overexpressing transgenic mice exhibit severely altered Vbeta T cell frequency and reduced Vbeta5.1/5.2 and Vbeta8.1/8.2/8.3 rearrangements, demonstrating that SMAR1 plays an important role in regulation of V(D)J recombination and T cell development in vivo. Transgenic mouse model, flow cytometry, PCR analysis of V(D)J rearrangements The Journal of biological chemistry Medium 15623522
2007 SMAR1 transcription is regulated by p53 through a p53 response element in the SMAR1 promoter; upon doxorubicin-induced DNA damage, acetylated p53 is recruited to the SMAR1 promoter, activating its transcription. In turn, SMAR1 inhibits tumor cell migration through inhibition of TGFbeta signaling and its downstream targets including cutl1 and focal adhesion molecules. ChIP, reporter assay, siRNA knockdown, migration assay PloS one Medium 17668048
2015 SMAR1 negatively regulates alternative splicing through HDAC6-mediated deacetylation of RNA-binding protein Sam68. SMAR1 is enriched in nuclear splicing speckles and associates with snRNAs involved in splice site recognition. ERK-1/2-mediated phosphorylation of SMAR1 at threonines 345 and 360 localizes SMAR1 to the cytoplasm, preventing its interaction with Sam68. Loss of SMAR1 increases Sam68 acetylation and CD44 variant exon inclusion, enhancing metastatic propensity. Co-IP, ChIP, CLIP, subcellular fractionation, phosphorylation-site mutagenesis, siRNA knockdown, in vivo tail-vein metastasis model Proceedings of the National Academy of Sciences of the United States of America High 26080397
2017 Cdc20, the substrate receptor of the APC/C ubiquitin ligase complex, binds SMAR1 and promotes its K48-linked polyubiquitylation and proteasomal degradation in a D-box motif-dependent manner. shRNA-mediated inactivation of Cdc20 leads to significant stabilization of SMAR1. Cdc20 fails to target SMAR1 upon genotoxic stress, allowing SMAR1 to support DNA damage repair. Cdc20-mediated degradation of SMAR1 promotes cell migration and invasion. Co-immunoprecipitation, ubiquitylation assay, shRNA knockdown, D-box mutants, Western blot Cell death & disease High 28617439
2014 SMAR1 inhibits EMT by two mechanisms: (1) transcriptional repression of Slug via direct recruitment of an SMAR1/HDAC1 complex to the MAR site in the Slug promoter, restoring E-cadherin expression; (2) hindering E-cadherin–MDM2 interaction, thereby reducing ubiquitination and degradation of E-cadherin protein. siRNA knockdown of SMAR1 results in coordinated Slug-mediated E-cadherin repression and MDM2-mediated E-cadherin degradation. ChIP, Co-IP, ubiquitination assay, siRNA knockdown, migration assay The Journal of biological chemistry High 25086032
2012 TCF-4, β-catenin, and SMAR1 tether together at the -143 nucleotide site on the HIV LTR to inhibit HIV promoter activity, likely by pulling the HIV DNA segment into the nuclear matrix away from transcriptional machinery. Deletion/mutation of this site or TCF-4/β-catenin knockdown enhanced basal HIV promoter activity ~5-fold. ChIP, reporter assay with deletion/mutation, siRNA knockdown Journal of virology Medium 22674979
2010 SMAR1 binds to the LTR MAR of HIV-1 and reinforces transcriptional silencing by tethering the LTR MAR to the nuclear matrix. The SMAR1-associated HDAC1-mSin3 corepressor complex is dislodged from the LTR upon cellular activation, increasing histone acetylation and RNA Pol II recruitment. SMAR1 overexpression reduces LTR-mediated transcription in both Tat-dependent and -independent manners, decreasing virion production. ChIP, nuclear fractionation (matrix tethering), reporter assay, Western blot for histone modifications Virology Medium 20153010
2008 SMAR1 binds to the MAR site in the IκBα promoter, recruits a corepressor complex, and represses IκBα transcription, resulting in formation of functional but phosphorylation-deficient and transactivation-deficient p65-p50 NF-κB complexes. SMAR1 down-regulates a subset of NF-κB target genes involved in tumorigenesis and inhibits TNFα-induced NF-κB activation independently of the classical pathway. ChIP, EMSA, reporter assay, NF-κB target gene array, overexpression and knockdown The Journal of biological chemistry Medium 18981184
2014 SMAR1 coordinates with HDAC6 to maintain Ku70 in a deacetylated state. SMAR1 knockdown results in enhanced Ku70 acetylation, impaired recruitment of Ku70 to chromatin fractions, and altered Bax-mediated apoptosis. Ionizing radiation induces SMAR1 expression and its redistribution as distinct nuclear foci via ATM-mediated phosphorylation at serine 370. SMAR1 regulates IR-induced G2/M arrest by facilitating Chk2 phosphorylation and provides radioresistance by modulating deacetylated Ku70 association with Bax. Co-IP, chromatin fractionation, siRNA knockdown, immunofluorescence, phosphorylation assay Cell death & disease Medium 25299772
2021 SMAR1 regulates PKM alternative splicing by recruiting HDAC6 to deacetylate PTBP1, which reduces PTBP1 enrichment on PKM pre-mRNA (measured by CLIP). This promotes PKM1 over PKM2 expression, suppresses the Warburg effect, and inhibits tumorigenesis in a PKM2-dependent manner. CLIP, immunoprecipitation (acetylation), qRT-PCR, Western blot, enzymatic assays, in vivo mouse tumor model Cancer & metabolism Medium 33863392
2010 SMAR1 directly interacts with and inhibits AKR1a4 enzyme activity in the cytoplasm. Upon stress, ATM kinase promotes nuclear translocation of SMAR1, causing dissociation of the SMAR1-AKR1a4 complex and elevated AKR1a4 activity. AKR1a4 enzyme activity is elevated in higher grades of breast cancer where SMAR1 is downregulated. Co-IP, enzyme activity assay, subcellular fractionation, ATM kinase assay The international journal of biochemistry & cell biology Medium 20097305
2015 SMAR1 negatively regulates STAT3 expression by binding to the MAR element of the STAT3 promoter adjacent to IL-6 response elements, favoring Foxp3 expression and Treg cell differentiation. T-cell-specific conditional knockdown of SMAR1 exhibits increased susceptibility to colitis and compromised Treg suppressor function with increased Th17 differentiation. ChIP, conditional SMAR1 knockout mice, flow cytometry, transfer colitis model Mucosal immunology Medium 25993445
2015 SMAR1 functions as a negative regulator of Th1 and Th17 differentiation by binding to MAR regions in the promoters of T-bet and IL-17, respectively. Conditional knockout of SMAR1 in T cells resulted in resistance to eosinophilic airway inflammation with skewing toward Th1 response. ChIP, conditional SMAR1 knockout mice (T-cell specific), flow cytometry, OVA allergic airway model Mucosal immunology Medium 25736456
2014 SMAR1 represses HPV18 E6 transcription by binding to MAR elements in the HPV18 LCR and E6 sequences, recruiting an SMAR1-HDAC1 repressor complex that decreases histone acetylation at H3K9 and H3K18 and inhibits c-Fos binding at AP-1 sites in the E6 promoter. ChIP, reporter assay, siRNA knockdown, histone modification analysis The Journal of biological chemistry Medium 25157104
2009 SMAR1 directly interacts with MDM2 and inhibits AKR1a4 enzyme activity. In addition, SMAR1 overexpression modulates cell surface roughness as measured by AFM, correlating with cytoskeletal protein expression changes seen by microarray. AFM/SEM morphology, microarray, overexpression/knockdown BMC cancer Low 19799771
2018 SMAR1 inhibits Wnt/β-catenin signaling by recruiting HDAC5 to the β-catenin promoter, resulting in reduced H3K9 acetylation, decreased β-catenin expression, and inhibited cell migration and invasion. During aberrant Wnt3a signaling, SMAR1 undergoes proteasomal degradation dependent on its D-box elements (RCHL and RQRL); substitution mutations in these D-box elements completely abrogated degradation. ChIP, reporter assay, siRNA knockdown, D-box mutagenesis, ITC, in vivo mouse tumor model Oncotarget Medium 29765542
2013 miR-320a negatively regulates SMAR1 expression by directly binding to its 3'UTR. In response to mild DNA damage, miR-320a expression decreases, resulting in enhanced SMAR1 protein levels. During hemin-induced erythroid differentiation, enhanced SMAR1 negatively correlates with miR-320a expression. SMAR1 in turn binds to the promoter of miR-221/222 to regulate early erythropoiesis. 3'UTR reporter assay, ChIP, miRNA inhibitor/mimic, siRNA knockdown, Western blot The international journal of biochemistry & cell biology Medium 23876508
2020 In breast cancer stem cells, SMAR1 expression is decreased through cooperative interaction of pluripotency factors Oct4 and Sox2 with HDAC1. Overexpression of SMAR1 sensitizes CSCs to chemotherapy through SMAR1-dependent recruitment of HDAC2 to the ABCG2 gene promoter, repressing its transcription. Aspirin restores SMAR1 expression and ABCG2 repression, enhancing chemosensitivity. ChIP, Co-IP, siRNA/overexpression, ABCG2 reporter assay, in vivo mouse tumor model Science signaling Medium 33082288
2007 SMAR1 mRNA is stabilized by a minor stem-loop structure in its 5'UTR (phi1 UTR) in response to Prostaglandin A2 (PGA2), forming a nucleoprotein complex that increases SMAR1 transcript and protein levels. Breast cancer cell lines express a variant 5'UTR (phi17 UTR) lacking this stem-loop, preventing PGA2-induced stabilization and resulting in low SMAR1 levels. RNA secondary structure analysis, RNA-protein binding assay, mRNA stability assay, reporter assay Nucleic acids research Medium 17726044
2010 HSP70 binds to a novel site on the phi1 SMAR1 5'UTR upon PGA2 treatment, stabilizing the wild-type SMAR1 transcript. HSP70 knockdown perturbs SMAR1-mediated cell cycle arrest in PGA2-treated cells. HSP70 cannot bind the phi17 SMAR1 UTR variant predominant in breast cancers, accounting for low SMAR1 protein levels. RNA immunoprecipitation, UV cross-link and immunoprecipitation, siRNA knockdown, cell cycle analysis FEBS letters Medium 20153327
2009 SMAR1 regulates TNFα-induced CD40 expression: SMAR1 recruits HDAC1 to the CD40 promoter to repress basal transcription; TNFα induces phosphorylation of SMAR1 at Ser-347, promoting its cytoplasmic translocation and releasing repression. Concomitantly, JAK1-mediated STAT1 phosphorylation at Tyr-701 drives nuclear STAT1 activation of CD40 via p300 recruitment. ChIP, reporter assay, phosphorylation assay, subcellular fractionation Biochemical and biophysical research communications Medium 20006573
2016 ChIP-sequencing revealed that SMAR1 binds to T(C/G) repeat sequences genome-wide, targeting genes in diverse biological pathways. SMAR1 binds and represses the miR-371-373 cluster promoter by recruiting an HDAC1/mSin3A complex; a ~200 bp promoter region is necessary for SMAR1 binding. SMAR1 regulation of miR-371-373 inhibits breast cancer tumorigenesis and metastasis in vivo. ChIP-seq, ChIP, reporter assay, SMAR1 overexpression/knockdown, in vivo tumor model Scientific reports Medium 27671416
2011 SMAR1 inhibits p53 acetylation and p53-dependent apoptosis by repressing p300 expression in response to DNA damage. SMAR1 interacts with the p53-p300 transcriptional complex and antagonizes p300 interaction with p53, suppressing activation of p53 apoptotic targets and miR-34a. Ectopic p300 expression rescues SMAR1-mediated inhibition on p53. Co-IP, ChIP, reporter assay, siRNA knockdown, Western blot for p53 acetylation The international journal of biochemistry & cell biology Medium 22074660
2024 ZNF471 interacts with BANP (demonstrated by Co-IP) in renal cancer cells and suppresses the malignant phenotype by inactivating the PI3K/AKT/mTOR signaling pathway. Co-immunoprecipitation, transcriptome sequencing, Western blot, functional cell biology assays International journal of biological sciences Low 38169650
2024 BANP overexpression in human umbilical vein endothelial cells promotes p53 phosphorylation and nuclear retention, inducing cellular senescence in the context of chronic intermittent hypoxia. Overexpression, cell cycle analysis, SA-β-gal staining, Western blot for p53 phosphorylation and nuclear fractionation Gerontology Low 38168028
2021 SMAR1 suppresses the cancer stem cell population in colorectal cancer by acting as a transcriptional repressor of hTERT. SMAR1 interacts with the HDAC1/mSin3a co-repressor complex at the hTERT promoter to mediate HDAC1-dependent transcriptional repression. Knockdown of SMAR1 promotes cancer stem cell phenotype and sphere-forming ability. ChIP, Co-IP, siRNA knockdown, sphere formation assay, reporter assay The international journal of biochemistry & cell biology Medium 34551340
2019 SMAR1 positively regulates MHC class I surface expression by transcriptionally repressing calnexin through binding to a short MAR region in the calnexin promoter and forming a repressor complex with GATA2 and HDAC1. Influenza A (H1N1) infection increases SMAR1 levels, resulting in reduced calnexin expression and increased MHC I presentation. ChIP, Co-IP, reporter assay, siRNA knockdown, flow cytometry for MHC I, viral infection assay Neoplasia (New York, N.Y.) Medium 31422285
2014 SMAR1 represses NF-κB-dependent IL-8 transcription by binding to the IL-8 promoter MAR and recruiting an HDAC1-dependent co-repressor complex. Additionally, SMAR1 antagonizes p300-mediated acetylation of RelA/p65, a modification required for IL-8 transactivation. ChIP, reporter assay, Co-IP, acetylation assay, siRNA knockdown The international journal of biochemistry & cell biology Medium 25239884
2021 SMAR1 negatively regulates adipogenesis by recruiting the HDAC1/mSin3a repressor complex to the PPARγ promoter, suppressing PPARγ expression and adipocyte differentiation. During adipogenesis, cdc20-mediated proteasomal degradation of SMAR1 permits PPARγ upregulation; knockdown of cdc20 stabilizes SMAR1 and reduces adipocyte differentiation. ChIP, reporter assay, Co-IP, siRNA knockdown, in vitro differentiation assay Biochimica et biophysica acta. Molecular and cell biology of lipids Medium 34450266
2022 TOPORS, induced via the TLR4-TRIF pathway by LPS, binds the SMAR1 promoter (shown by ChIP) and modulates SMAR1 transcription. LPS-induced SMAR1 expression decreases STAT3 expression and skews tumor-associated macrophage polarization toward the M1 phenotype. ChIP, siRNA knockdown, reporter assay, macrophage polarization assay Molecular oncology Medium 34689394
2023 RBX1, an E3 ubiquitin ligase, degrades SMAR1 through the ubiquitin-proteasome pathway in anaplastic thyroid carcinoma cells, thereby disrupting the SMAR1/HDAC6 complex, leading to increased PKM2 expression, enhanced Warburg effect, and increased ATC cell metastasis. Co-IP, ubiquitination assay, siRNA knockdown, overexpression, metabolic assays Cell & bioscience Medium 36810109

Source papers

Stage 0 corpus · 70 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 Circular BANP, an upregulated circular RNA that modulates cell proliferation in colorectal cancer. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 145 28103507
2005 Tumor suppressor SMAR1 mediates cyclin D1 repression by recruitment of the SIN3/histone deacetylase 1 complex. Molecular and cellular biology 98 16166625
2018 CircRNA circ-BANP-mediated miR-503/LARP1 signaling contributes to lung cancer progression. Biochemical and biophysical research communications 83 29969631
2014 Inhibition of epithelial to mesenchymal transition by E-cadherin up-regulation via repression of slug transcription and inhibition of E-cadherin degradation: dual role of scaffold/matrix attachment region-binding protein 1 (SMAR1) in breast cancer cells. The Journal of biological chemistry 81 25086032
2021 BANP opens chromatin and activates CpG-island-regulated genes. Nature 71 34234345
2003 Direct interaction with and activation of p53 by SMAR1 retards cell-cycle progression at G2/M phase and delays tumor growth in mice. International journal of cancer 69 12494467
2010 Coordinated regulation of p53 apoptotic targets BAX and PUMA by SMAR1 through an identical MAR element. The EMBO journal 55 20075864
2014 Capsaicin-induced activation of p53-SMAR1 auto-regulatory loop down-regulates VEGF in non-small cell lung cancer to restrain angiogenesis. PloS one 54 24926985
2007 p53 target gene SMAR1 is dysregulated in breast cancer: its role in cancer cell migration and invasion. PloS one 54 17668048
2000 SMAR1, a novel, alternatively spliced gene product, binds the Scaffold/Matrix-associated region at the T cell receptor beta locus. Genomics 52 10950932
2017 Cdc20 directs proteasome-mediated degradation of the tumor suppressor SMAR1 in higher grades of cancer through the anaphase promoting complex. Cell death & disease 50 28617439
2012 Identification of novel T cell factor 4 (TCF-4) binding sites on the HIV long terminal repeat which associate with TCF-4, β-catenin, and SMAR1 to repress HIV transcription. Journal of virology 47 22674979
2009 Tumor suppressor protein SMAR1 modulates the roughness of cell surface: combined AFM and SEM study. BMC cancer 47 19799771
2015 Nuclear matrix-associated protein SMAR1 regulates alternative splicing via HDAC6-mediated deacetylation of Sam68. Proceedings of the National Academy of Sciences of the United States of America 43 26080397
2004 SMAR1 and Cux/CDP modulate chromatin and act as negative regulators of the TCRbeta enhancer (Ebeta). Nucleic acids research 36 15371550
2010 Gene regulation by SMAR1: Role in cellular homeostasis and cancer. Biochimica et biophysica acta 34 20709157
2005 Tumor suppressor SMAR1 activates and stabilizes p53 through its arginine-serine-rich motif. The Journal of biological chemistry 31 15701641
2014 Nuclear matrix protein SMAR1 represses c-Fos-mediated HPV18 E6 transcription through alteration of chromatin histone deacetylation. The Journal of biological chemistry 29 25157104
2010 Nuclear matrix protein SMAR1 represses HIV-1 LTR mediated transcription through chromatin remodeling. Virology 27 20153010
2021 Tumor suppressor SMAR1 regulates PKM alternative splicing by HDAC6-mediated deacetylation of PTBP1. Cancer & metabolism 26 33863392
2007 SMAR1-derived P44 peptide retains its tumor suppressor function through modulation of p53. The Journal of biological chemistry 26 17229733
2009 SMAR1 forms a ternary complex with p53-MDM2 and negatively regulates p53-mediated transcription. Journal of molecular biology 25 19303885
2021 Circular RNA Circ-BANP Regulates Oxidized Low-density Lipoprotein-induced Endothelial Cell Injury Through Targeting the miR-370/Thioredoxin-interacting Protein Axis. Journal of cardiovascular pharmacology 23 33298736
2020 SMAR1 repression by pluripotency factors and consequent chemoresistance in breast cancer stem-like cells is reversed by aspirin. Science signaling 23 33082288
2018 SMAR1 inhibits Wnt/β-catenin signaling and prevents colorectal cancer progression. Oncotarget 23 29765542
2014 SMAR1 coordinates HDAC6-induced deacetylation of Ku70 and dictates cell fate upon irradiation. Cell death & disease 23 25299772
2004 Abnormal V(D)J recombination of T cell receptor beta locus in SMAR1 transgenic mice. The Journal of biological chemistry 22 15623522
2008 Tumor suppressor SMAR1 represses IkappaBalpha expression and inhibits p65 transactivation through matrix attachment regions. The Journal of biological chemistry 21 18981184
2015 Nuclear matrix protein SMAR1 control regulatory T-cell fate during inflammatory bowel disease (IBD). Mucosal immunology 20 25993445
2013 miR-320a regulates erythroid differentiation through MAR binding protein SMAR1. The international journal of biochemistry & cell biology 20 23876508
2000 Identification and molecular analysis of BANP. Gene 18 10940556
2015 Nuclear matrix binding protein SMAR1 regulates T-cell differentiation and allergic airway disease. Mucosal immunology 16 25736456
2023 RBX1 regulates PKM alternative splicing to facilitate anaplastic thyroid carcinoma metastasis and aerobic glycolysis by destroying the SMAR1/HDAC6 complex. Cell & bioscience 15 36810109
2022 Banp regulates DNA damage response and chromosome segregation during the cell cycle in zebrafish retina. eLife 15 35942692
2019 SMAR1 favors immunosurveillance of cancer cells by modulating calnexin and MHC I expression. Neoplasia (New York, N.Y.) 15 31422285
2017 Control of apoptosis by SMAR1. Molecular bioSystems 13 27934984
2012 Regulation of GAD65 expression by SMAR1 and p53 upon Streptozotocin treatment. BMC molecular biology 13 22978699
2011 Chromatin remodelling protein SMAR1 inhibits p53 dependent transactivation by regulating acetyl transferase p300. The international journal of biochemistry & cell biology 13 22074660
2010 SMAR1 regulates free radical stress through modulation of AKR1a4 enzyme activity. The international journal of biochemistry & cell biology 13 20097305
2016 SMAR1 binds to T(C/G) repeat and inhibits tumor progression by regulating miR-371-373 cluster. Scientific reports 12 27671416
2007 Stabilization of SMAR1 mRNA by PGA2 involves a stem loop structure in the 5' UTR. Nucleic acids research 12 17726044
2010 Heat-shock protein 70 binds to a novel sequence in 5' UTR of tumor suppressor SMAR1 and regulates its mRNA stability upon Prostaglandin A2 treatment. FEBS letters 11 20153327
2008 Tumor suppressor SMAR1 downregulates Cytokeratin 8 expression by displacing p53 from its cognate site. The international journal of biochemistry & cell biology 11 18822384
2024 ZNF471 Interacts with BANP to Reduce Tumour Malignancy by Inactivating PI3K/AKT/mTOR Signalling but is Frequently Silenced by Aberrant Promoter Methylation in Renal Cell Carcinoma. International journal of biological sciences 10 38169650
2022 Circular BANP knockdown inhibits the malignant progression of residual hepatocellular carcinoma after insufficient radiofrequency ablation. Chinese medical journal 10 34985013
2017 Chromatin Remodeling Protein SMAR1 Is a Critical Regulator of T Helper Cell Differentiation and Inflammatory Diseases. Frontiers in immunology 10 28232831
2014 Overexpression of SMAR1 Enhances Radiosensitivity in Human Breast Cancer Cell Line MCF7 via Activation of p53 Signaling Pathway. Oncology research 10 26629941
2024 SMAR1 and p53-regulated lncRNA RP11-431M3.1 enhances HIF1A translation via miR-138 in colorectal cancer cells under oxidative stress. The FEBS journal 9 39240540
2022 SMAR1 inhibits proliferation, EMT and Warburg effect of bladder cancer cells by suppressing the activity of the Wnt/β-catenin signaling pathway. Cell cycle (Georgetown, Tex.) 9 35980125
2023 Structural insights into DNA recognition by the BEN domain of the transcription factor BANP. The Journal of biological chemistry 8 37086783
2016 Carbon nanospheres mediated delivery of nuclear matrix protein SMAR1 to direct experimental autoimmune encephalomyelitis in mice. International journal of nanomedicine 8 27274234
2014 Chromatin remodeling protein SMAR1 regulates NF-κB dependent Interleukin-8 transcription in breast cancer. The international journal of biochemistry & cell biology 8 25239884
2021 SMAR1 attenuates the stemness of osteosarcoma cells via through suppressing ABCG2 transcriptional activity. Environmental toxicology 7 33543840
2015 MAR binding protein SMAR1 favors IL-10 mediated regulatory T cell function in acute colitis. Biochemical and biophysical research communications 7 26168735
2022 RING finger protein TOPORS modulates the expression of tumor suppressor SMAR1 in colorectal cancer via the TLR4-TRIF pathway. Molecular oncology 6 34689394
2022 The transcriptomic landscape of elderly acute myeloid leukemia identifies B7H3 and BANP as a favorable signature in high-risk patients. Frontiers in oncology 6 36505804
2009 Tumor Necrosis Factor alpha (TNFalpha) regulates CD40 expression through SMAR1 phosphorylation. Biochemical and biophysical research communications 6 20006573
2024 BANP Participates in the Chronic Intermittent Hypoxia-Induced Senescence of Vascular Endothelial Cells by Promoting P53 Phosphorylation and Nuclear Retention. Gerontology 5 38168028
2021 Chromatin remodeling protein SMAR1 regulates adipogenesis by modulating the expression of PPARγ. Biochimica et biophysica acta. Molecular and cell biology of lipids 5 34450266
2018 Carbon nanospheres mediated nuclear delivery of SMAR1 protein (DNA binding domain) controls breast tumor in mice model. Nanomedicine (London, England) 4 29338617
2024 Pre-clinical Evaluation of Karanjin Against DMBA-Induced Breast Cancer in Female Sprague-Dawley Rats Through Modulation of SMAR1 and CDP/CUx genes. Naunyn-Schmiedeberg's archives of pharmacology 2 39177785
2018 SMAR1 promotes immune escape of Tri-negative Breast Cancer through a mechanism involving T-bet/PD-1 Axis. Cellular and molecular biology (Noisy-le-Grand, France) 2 30301506
2015 Regulation of T cell lineage commitment by SMAR1 during inflammatory & autoimmune diseases. The Indian journal of medical research 2 26609032
2015 Constitutive expression of SMAR1 confers susceptibility to Mycobacterium tuberculosis infection in a transgenic mouse model. The Indian journal of medical research 2 26831422
2009 Modulation of chromatin by MARs and MAR binding oncogenic transcription factor SMAR1. Molecular and cellular biochemistry 2 19802523
2021 SMAR1 suppresses the cancer stem cell population via hTERT repression in colorectal cancer cells. The international journal of biochemistry & cell biology 1 34551340
2024 Structural basis of DNA recognition by BEN domain proteins reveals a role for oligomerization in unmethylated DNA selection by BANP. Nucleic acids research 0 39225042
2023 Nuclear Matrix-associated Protein SMAR1 Attenuated Acute Graft-versus-host Disease by Targeting JAK-STAT Signaling in CD4 + T Cells. Transplantation 0 37817309
2020 Correction to: Regulation of GAD65 expression by SMAR1 and p53 upon Streptozotocin treatment. BMC molecular and cell biology 0 32807076
2016 Genome-wide association study of copy number variation with lung function identifies a novel signal of association near BANP for forced vital capacity. BMC genetics 0 27514831

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