Affinage

SNIP1

Smad nuclear-interacting protein 1 · UniProt Q8TAD8

Length
396 aa
Mass
45.8 kDa
Annotated
2026-06-10
39 papers in source corpus 18 papers cited in narrative 18 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

SNIP1 is a nuclear FHA-domain protein that integrates transcriptional control, mRNA processing, and chromatin regulation, originally identified as a competitive inhibitor of CBP/p300-dependent signaling (PMID:10887155). Through its N-terminus it binds the C/H1 domain of CBP/p300 and blocks coactivator access for both Smad4-dependent TGF-β signaling and the NF-κB subunit RelA/p65, while sparing p300 targets that engage other domains (PMID:10887155, PMID:11567019). Conversely, its C-terminus binds c-MYC, stabilizing the oncoprotein against proteasomal and SKP2-mediated ubiquitination and bridging it to p300/KAT2A coactivators to enhance c-MYC-driven transcription and oncogenic transformation (PMID:17157259, PMID:37726400). SNIP1 also acts as a chromatin scaffold, bridging the dioxygenase TET2 to c-MYC target promoters and to HDAC1/2 to repress specific genes, and restricting PRC2 recruitment and H3K27me3 turnover during neurogenesis (PMID:30404004, PMID:37553330, PMID:40067382). In RNA processing, SNIP1 is a core subunit of the SSRC complex (with SkIP, THRAP3, BCLAF1, Pinin) that recruits U2AF65 to stabilize cyclin D1 mRNA, and its FHA domain reads CDK11-phosphorylated SF3B1 to recruit the RES complex during spliceosome activation (PMID:18794151, PMID:41904131). SNIP1 abundance and activity are tuned by KMT5A-mediated K301 mono-methylation, MKRN1-mediated ubiquitin-proteasomal degradation, and SENP1-regulated SUMOylation (PMID:35449131, PMID:37620897, PMID:38309408). A biallelic E366G variant in the FHA domain causes an autosomal recessive neurodevelopmental disorder by impairing phospho-SF3B1 binding and pre-mRNA splicing (PMID:34570759, PMID:41904131).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2000 High

    Established the founding mechanism: how a nuclear factor could selectively dampen TGF-β transcriptional output, by showing SNIP1 sequesters CBP/p300 from Smad4.

    Evidence Yeast two-hybrid, endogenous reciprocal Co-IP, in vitro binding, reporter assays and Xenopus rescue in NMuMg cells

    PMID:10887155

    Open questions at the time
    • Did not address whether the same competition operates on other p300-dependent pathways
    • No structural basis for the N-terminus/CBP interaction
  2. 2001 High

    Generalized the competitive-inhibition model to a second pathway, showing SNIP1 also blocks RelA/p65 access to the C/H1 domain of CBP/p300, defining it as a selective coactivator-sequestering regulator rather than a TGF-β-specific factor.

    Evidence Domain mapping, competitive binding assays, reporter assays with transcription-factor controls, immunohistochemistry

    PMID:11567019

    Open questions at the time
    • Selectivity rules for which p300-binding factors are inhibited not fully defined
    • In vivo relevance to NF-κB-driven programs untested
  3. 2004 High

    Connected SNIP1 to cell-cycle progression, showing its loss arrests cells in G1 with loss of cyclin D1 and linking it to SWI/SNF (BRG1) chromatin remodeling.

    Evidence siRNA knockdown, flow cytometry, RT-PCR, cyclin D1 promoter reporter, Co-IP with BRG1 in human cell lines

    PMID:15378006

    Open questions at the time
    • Whether cyclin D1 control was transcriptional vs post-transcriptional was unresolved (later revised)
    • BRG1 interaction not functionally dissected
  4. 2006 High

    Reframed SNIP1 as a pro-oncogenic c-MYC cofactor, showing its C-terminus stabilizes c-MYC against degradation and bridges c-MYC to p300, cooperating in transformation.

    Evidence Yeast two-hybrid, Co-IP, proteasomal degradation assay, focus formation and soft-agar assays, tissue arrays

    PMID:17157259

    Open questions at the time
    • E3 ligase opposed by SNIP1 not identified at this stage
    • Mechanism of degradation protection unresolved
  5. 2007 Medium

    Linked SNIP1 to genome-stability signaling, showing it is required for ATR-dependent phosphorylation of p53, Chk1 and H2AX and for p14ARF function, independent of its cyclin D1 role.

    Evidence siRNA knockdown, phospho-substrate immunoblots after UV, reporter assays in U-2 OS cells

    PMID:17260016

    Open questions at the time
    • Direct molecular role of SNIP1 in the ATR pathway not defined
    • Single lab, not independently confirmed
  6. 2008 High

    Revised the cyclin D1 mechanism: rather than acting at the promoter, SNIP1 stabilizes cyclin D1 mRNA as part of the SSRC RNA-processing complex that recruits U2AF65, establishing a co/post-transcriptional function.

    Evidence Co-IP complex isolation, RNA-IP, ChIP, siRNA, mRNA stability assays

    PMID:18794151

    Open questions at the time
    • Generality of SSRC-stabilized transcripts beyond cyclin D1 unknown
    • How SSRC selects target RNAs not defined
  7. 2008 High

    Provided the structural and complex-context basis for SNIP1's FHA domain via its yeast ortholog Pml1, showing it is a near-pure FHA domain that integrates into the RES splicing complex through Snu17/Bud13 contacts.

    Evidence X-ray crystallography, recombinant RES reconstitution, truncation/mutagenesis, splice-site assays in yeast

    PMID:19033360

    Open questions at the time
    • FHA phosphopeptide-binding pocket appeared dispensable in yeast, leaving its functional role open (resolved later in human)
    • Human RES architecture inferred from yeast
  8. 2011 Low

    Reported SNIP1 subnuclear speckle localization and a candidate role in activating heat-shock gene transcription.

    Evidence EGFP fusion microscopy, HSE-luciferase reporter, RT-PCR for HSP70A1A/HSP27 in HeLa/HEK293/H1299 (overexpression)

    PMID:22020748

    Open questions at the time
    • Overexpression reporter only, no endogenous validation
    • Mechanism of HSE activation undefined
  9. 2018 High

    Defined SNIP1 as a chromatin scaffold bridging TET2 to c-MYC target promoters, coupling it to DNA-damage-response gene regulation and apoptosis protection.

    Evidence Mammalian two-hybrid, reciprocal Co-IP, ChIP, siRNA, DNA-damage apoptosis assays

    PMID:30404004

    Open questions at the time
    • Whether TET2 catalytic activity is required at these loci not addressed here
    • Genome-wide scope of the ternary complex limited
  10. 2021 Medium

    Showed an lncRNA-directed route to c-MYC stabilization, with AFAP1-AS1 binding SNIP1 to suppress c-MYC ubiquitination and drive EMT/metastasis.

    Evidence RNA pull-down/MS, Co-IP, ubiquitination assay, in vivo lung metastasis model

    PMID:34168109

    Open questions at the time
    • SNIP1 mechanism secondary to the lncRNA focus
    • Direct lncRNA-SNIP1 interface not mapped
  11. 2021 Medium

    Provided human in vivo proof of essentiality: a biallelic SNIP1 E366G variant causes autosomal recessive neurodevelopmental disease with altered neurodevelopmental gene expression.

    Evidence Human genetic study and transcriptome profiling in affected Amish individuals

    PMID:34570759

    Open questions at the time
    • Molecular consequence of E366G not resolved at this stage (later linked to phospho-SF3B1 binding)
    • Mechanism limited to expression changes
  12. 2022 High

    Identified a methylation switch controlling SNIP1 cofactor partner choice, with KMT5A mono-methylating K301 to release KAT2A and route the c-MYC/KAT2A complex to pro-metastatic targets.

    Evidence In vitro methylation, MS site mapping, K301 mutagenesis, Co-IP, ChIP, xenograft model

    PMID:35449131

    Open questions at the time
    • Demethylase reversing K301 not identified
    • Breadth of methylation-controlled target genes limited
  13. 2023 High

    Established SNIP1 as a restrictor of PRC2 activity in neurogenesis, with its loss causing PRC2-dependent caspase-9 apoptosis and brain dysplasia rescued by PRC2 depletion.

    Evidence Conditional knockout, ChIP-seq for PRC2/H3K27me3, genetic epistasis, apoptosis assays in mouse brain

    PMID:37553330

    Open questions at the time
    • How SNIP1 mechanistically limits PRC2 occupancy unresolved
    • Link to splicing role not integrated
  14. 2023 High

    Defined a degradation arm regulating SNIP1, with MKRN1 ubiquitinating SNIP1 to de-repress TGF-β signaling and promote colorectal cancer EMT/metastasis.

    Evidence Ubiquitination assay, quantitative/ubiquitination proteomics, Co-IP, conditional KO mouse, invasion assays

    PMID:37620897

    Open questions at the time
    • Signals controlling MKRN1 activity toward SNIP1 unknown
    • Ubiquitination site on SNIP1 not mapped
  15. 2023 Medium

    Extended SNIP1's c-MYC-stabilizing function to an m6A-reader role, forming a ternary complex with c-MYC and m6A-modified BCAN-AS1 to block SKP2-mediated c-MYC degradation.

    Evidence RNA pull-down, Co-IP, m6A detection, ubiquitination assay, MS in pancreatic cancer cells

    PMID:37726400

    Open questions at the time
    • m6A-reader claim from a single lab
    • Structural basis of m6A recognition by SNIP1 unknown
  16. 2024 Medium

    Added SUMOylation as a third PTM layer, with SENP1 deSUMOylating SNIP1 and MSC-AS1 sequestering SENP1 to inhibit SNIP1 and promote EMT/intestinal fibrosis.

    Evidence Co-IP, SUMOylation assay, siRNA, TNBS colitis mouse model

    PMID:38309408

    Open questions at the time
    • SNIP1 SUMOylation site and functional consequence not fully defined
    • Novel PTM claim from single lab
  17. 2025 High

    Generalized the TET2 scaffold function to repressive chromatin, showing SNIP1 is indispensable for bridging TET2 to HDAC1/2 to deacetylate H3K27ac and silence RUNX2, with SNIP1 loss accelerating vascular calcification.

    Evidence Co-IP of ternary complex, TET2 catalytic-dead mutant, ChIP for H3K27ac, siRNA, in vivo calcification models

    PMID:40067382

    Open questions at the time
    • How SNIP1 selects TET2/HDAC target loci unknown
    • Relationship to SNIP1's c-MYC/TET2 role not unified
  18. 2026 High

    Resolved the long-open FHA function and the disease mechanism, showing the FHA domain reads CDK11-phosphorylated SF3B1 to recruit the RES complex during spliceosome activation, with the E366G variant abrogating this binding.

    Evidence Quantitative spliceosome proteomics, iCLIP-seq, CDK11 inhibition, FHA/E366G mutagenesis, acute depletion and splicing assays

    PMID:41904131

    Open questions at the time
    • How splicing role mechanistically connects to SNIP1's transcriptional/chromatin functions
    • Full set of SNIP1-dependent splicing events not catalogued

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how SNIP1's distinct activities — CBP/p300 sequestration, c-MYC stabilization, TET2/PRC2 chromatin scaffolding, and phospho-SF3B1/RES-dependent splicing — are coordinated within one protein and which is primary to its essential and neurodevelopmental roles.
  • No integrated model linking the splicing and transcriptional/chromatin functions
  • PTM crosstalk (methylation, ubiquitination, SUMOylation) governing function-switching not mapped
  • Structure of human SNIP1 in complex with partners beyond the FHA domain lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 3 GO:0060090 molecular adaptor activity 3 GO:0140110 transcription regulator activity 3 GO:0098772 molecular function regulator activity 2 GO:0042393 histone binding 1
Localization
GO:0005654 nucleoplasm 3 GO:0005634 nucleus 2
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-4839726 Chromatin organization 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-8953854 Metabolism of RNA 2
Partners
CBP/P300HDAC1KAT2AMYCRELASF3B1SMAD4TET2
Complex memberships
RES complexSSRC complex

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 SNIP1 is a nuclear protein containing an NLS and FHA domain. Its C-terminus interacts with Smad1 and Smad2, while its N-terminus binds both Smad4 and the coactivator CBP/p300. Endogenous SNIP1 co-immunoprecipitates with Smad4 and CBP/p300 in NMuMg cells, and in vitro binding was confirmed. Overexpression of SNIP1 or its N-terminus inhibits Smad4/p300 complex formation and suppresses TGF-β-induced transcriptional activation, identifying SNIP1 as a nuclear inhibitor of CBP/p300-dependent TGF-β signaling. Yeast two-hybrid, mammalian co-immunoprecipitation (endogenous and overexpression), in vitro binding assay, reporter gene assay, Xenopus developmental rescue experiments Genes & development High 10887155
2001 SNIP1 inhibits NF-κB transcriptional activity by competing with the NF-κB subunit RelA/p65 for binding to the C/H1 domain of CBP/p300. This inhibition is mediated by the N-terminal domain of SNIP1 and is selective: SNIP1 does not interfere with p53 (which binds other p300 domains) or CBP/p300-independent factors such as VP16. Immunohistochemistry showed co-localization of SNIP1 with RelA/p65 and p300 in specific tissues. Reporter gene assay, domain mapping (N-terminal SNIP1 constructs), competitive binding assay, immunohistochemistry The Journal of biological chemistry High 11567019
2004 siRNA-mediated knockdown of SNIP1 in human cell lines causes G1 cell cycle arrest, reduced cell proliferation, and decreased cyclin D1 mRNA and protein levels. SNIP1 depletion inhibits cyclin D1 promoter activity in a manner dependent on an AP-1 binding site. SNIP1 itself is induced by serum stimulation prior to cyclin D1 expression. An interaction with BRG1, a component of the SWI/SNF chromatin remodelling complex, was detected. These effects were independent of p53 and Rb. siRNA knockdown, flow cytometry (cell cycle analysis), RT-PCR, reporter gene assay, co-immunoprecipitation (SNIP1-BRG1) Oncogene High 15378006
2006 SNIP1 associates with c-Myc via its C-terminus binding to the N-terminus of c-Myc, as identified by yeast two-hybrid and confirmed in mammalian cells. SNIP1 enhances c-Myc transcriptional activity by: (1) stabilizing c-Myc against proteasomal degradation, and (2) bridging the c-Myc/p300 complex. SNIP1 synergizes with c-Myc and H-Ras in oncogenic focus formation and anchorage-independent growth assays. Yeast two-hybrid, co-immunoprecipitation, proteasomal degradation assay, in vitro transformation/focus formation assay, soft agar colony assay, tissue array co-staining Molecular cell High 17157259
2007 SNIP1 is required for ATR checkpoint kinase-dependent signaling in human U-2 OS cells: SNIP1 depletion impairs p53 induction in response to UV irradiation and selectively reduces phosphorylation of ATR targets including p53, Chk1, and H2AX. SNIP1 is also required for ATR-dependent functions of the p14(ARF) tumor suppressor, including p14(ARF)-mediated modulation of RelA(p65) NF-κB activity. These functions are independent of SNIP1's role in regulating cyclin D1. siRNA knockdown, immunoblot for phosphorylation of ATR substrates (p53, Chk1, H2AX), UV irradiation treatment, reporter gene assay Oncogene Medium 17260016
2008 The majority of nucleoplasmic SNIP1 resides in a complex (termed SNIP1/SkIP-associated RNA-processing complex, SSRC) containing SkIP, THRAP3, BCLAF1, and Pinin — proteins with roles in RNA processing and transcriptional regulation. SNIP1 does not primarily regulate cyclin D1 transcription but instead stabilizes cyclin D1 mRNA through a cotranscriptional or post-transcriptional mechanism. The SSRC complex is coordinately recruited to the 3' end of the cyclin D1 gene and to cyclin D1 RNA. SNIP1 is required for recruitment of the RNA processing factor U2AF65 to both the cyclin D1 gene and RNA. Co-immunoprecipitation (complex isolation), RNA co-immunoprecipitation, chromatin immunoprecipitation (ChIP), siRNA knockdown, mRNA stability assays Cancer research High 18794151
2008 The yeast ortholog of SNIP1, Pml1, is a component of the RES splicing complex. X-ray crystallography revealed Pml1 consists mainly of an FHA domain. Mutation of the putative phosphothreonine-binding pocket of Pml1's FHA domain does not affect pre-mRNA splicing. Pml1 integrates into the RES complex by binding Snu17, which itself contacts Bud13; mutagenesis and truncation studies demarcated the binding sites within these subunits. X-ray crystallography, recombinant complex reconstitution, truncation and mutagenesis, alternative splice-site choice assay Nucleic acids research High 19033360
2011 Overexpression of SNIP1-EGFP in HeLa cells shows nuclear localization with characteristic subnuclear distribution in speckles or larger discrete nuclear bodies. Overexpression of SNIP1 in HEK293 or H1299 cells strongly activates the HSE (heat shock element) signaling pathway reporter, and SNIP1 selectively regulates transcription of HSP70A1A and HSP27. Fluorescence microscopy (EGFP fusion), reporter gene assay (HSE-luciferase), RT-PCR (HSP70A1A, HSP27) Molecular and cellular biochemistry Low 22020748
2018 SNIP1 physically interacts with TET2 DNA dioxygenase and bridges TET2 to bind the transcription factor c-MYC, as identified by mammalian two-hybrid screen and confirmed by co-immunoprecipitation. SNIP1 recruits TET2 to promoters of c-MYC target genes including those involved in DNA damage response. TET2-mediated protection from DNA damage-induced apoptosis requires SNIP1. Mammalian two-hybrid screen, co-immunoprecipitation, chromatin immunoprecipitation (ChIP), siRNA knockdown, apoptosis assays (DNA damage) Cell reports High 30404004
2021 SNIP1 inhibits ubiquitination and degradation of c-Myc protein. The lncRNA AFAP1-AS1 interacts with SNIP1 (identified by RNA pull-down and mass spectrometry), and this interaction promotes stabilization of c-Myc, which in turn upregulates ZEB1, ZEB2, and SNAIL to enhance EMT and lung cancer metastasis. RNA pull-down, mass spectrometry, co-immunoprecipitation, ubiquitination assay, in vivo lung metastasis model Signal transduction and targeted therapy Medium 34168109
2021 A biallelic SNIP1 variant (p.Glu366Gly) in the Amish community causes an autosomal recessive neurodevelopmental disorder. Gene transcript studies in affected individuals defined altered expression profiles of molecules with neurodevelopmental roles, confirming SNIP1's role in human spliceosome function and TGF-β signal transduction in vivo. Human genetic study (biallelic variant identification), gene expression profiling in affected individuals PLoS genetics Medium 34570759
2022 SNIP1 is a non-histone substrate of the lysine methyltransferase KMT5A. KMT5A mono-methylates SNIP1 at K301. This methylation releases the histone acetyltransferase KAT2A from SNIP1, promotes interaction of c-MYC with KAT2A, and recruits the c-MYC/KAT2A complex to promoters of c-MYC targets. This cascade inhibits the Hippo kinase pathway and transcriptionally activates MARK4 to enhance TNBC metastasis. In vitro methylation assay, mass spectrometry (methylation site identification), co-immunoprecipitation, ChIP, site-directed mutagenesis (K301), xenograft mouse model Nature communications High 35449131
2023 SNIP1 is required for recruitment of PRC2 to target gene loci and for H3K27me3 turnover in neural progenitor cells. SNIP1-depleted mouse brains exhibit dysplasia with robust caspase 9-dependent apoptosis. Depletion of PRC2 is sufficient to reduce apoptosis and brain dysplasia in SNIP1-depleted brains, establishing a genetic epistasis where SNIP1 normally restricts PRC2 activity at survival/neurogenesis gene loci. Conditional knockout (in vivo), ChIP-seq (PRC2/H3K27me3 occupancy), epistasis (double depletion of SNIP1 and PRC2), caspase 9 apoptosis assay Nature communications High 37553330
2023 MKRN1 (an E3 ubiquitin ligase) ubiquitinates and degrades SNIP1. Loss of SNIP1 protein de-represses TGF-β signaling, promoting EMT in colorectal cancer cells. Intestinal conditional knockout of MKRN1 in mice reduces intestinal lesions and metastatic liver microlesions, consistent with the MKRN1/SNIP1/TGF-β axis driving metastasis. Ubiquitination assay, quantitative proteomics, ubiquitination modification omics, co-immunoprecipitation, conditional knockout mouse model, in vitro proliferation/invasion assays Journal of experimental & clinical cancer research High 37620897
2023 SNIP1 forms a ternary complex with c-MYC and lncRNA BCAN-AS1 (via SNIP1 recognizing N6-methyladenosine modification on BCAN-AS1). This complex blocks SKP2-mediated ubiquitination and degradation of c-MYC, thereby stabilizing c-MYC protein in pancreatic cancer cells. RNA pull-down, co-immunoprecipitation, m6A modification detection, ubiquitination assay, mass spectrometry Cell death and differentiation Medium 37726400
2024 SNIP1 SUMOylation is regulated by SENP1 deSUMOylation activity. The lncRNA MSC-AS1 binds SENP1 and blocks its deSUMOylation of SNIP1, thereby inhibiting SNIP1 activity and promoting EMT and intestinal fibrosis in Crohn's disease. Co-immunoprecipitation (MSC-AS1/SENP1/SNIP1), SUMOylation assay, siRNA knockdown, in vivo mouse model (TNBS-induced colitis) International journal of biological macromolecules Medium 38309408
2025 TET2 forms an inhibitory complex with HDAC1/2 and SNIP1 to suppress RUNX2 transcription at its P2 promoter in vascular smooth muscle cells; this function is independent of TET2's catalytic demethylase activity. SNIP1 is indispensable for TET2's interaction with HDAC1/2 (i.e., SNIP1 bridges TET2 to HDAC1/2), and knockdown of SNIP1 accelerates vascular calcification in mice. TET2 deacetylates H3K27ac at the RUNX2 P2 promoter through this complex. Co-immunoprecipitation (TET2/HDAC1/2/SNIP1 complex), enzymatic loss-of-function mutation of TET2, ChIP (H3K27ac), siRNA knockdown, in vivo mouse models (vitamin D3 and CKD diet) The Journal of clinical investigation High 40067382
2026 The FHA domain of SNIP1 directly recognizes phosphorylated SF3B1 (P-SF3B1), phosphorylated by CDK11 during spliceosome activation. This interaction promotes recruitment of the RES (retention and splicing) complex during spliceosome activation. Acute SNIP1 depletion disrupts RES complex incorporation into spliceosomes, causes widespread splicing defects, promotes hyperphosphorylation of SF3B1 by CDK11, and impairs cell viability. The neurodevelopmental disorder-associated SNIP1 E366G variant impairs P-SF3B1 binding, pre-mRNA splicing, and cell viability. Quantitative proteomics of chromatin-associated spliceosomes, iCLIP-seq, CDK11 inhibitor (OTS964) treatment, FHA domain mutagenesis (including E366G disease variant), acute SNIP1 depletion, splicing assays Nature communications High 41904131

Source papers

Stage 0 corpus · 39 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2000 A novel smad nuclear interacting protein, SNIP1, suppresses p300-dependent TGF-beta signal transduction. Genes & development 111 10887155
2008 Regulation of cyclin D1 RNA stability by SNIP1. Cancer research 82 18794151
2021 Long non-coding RNA AFAP1-AS1 accelerates lung cancer cells migration and invasion by interacting with SNIP1 to upregulate c-Myc. Signal transduction and targeted therapy 78 34168109
2018 SNIP1 Recruits TET2 to Regulate c-MYC Target Genes and Cellular DNA Damage Response. Cell reports 77 30404004
2001 SNIP1 inhibits NF-kappa B signaling by competing for its binding to the C/H1 domain of CBP/p300 transcriptional co-activators. The Journal of biological chemistry 64 11567019
2006 SNIP1 is a candidate modifier of the transcriptional activity of c-Myc on E box-dependent target genes. Molecular cell 58 17157259
2022 KMT5A-methylated SNIP1 promotes triple-negative breast cancer metastasis by activating YAP signaling. Nature communications 50 35449131
2004 The FHA domain protein SNIP1 is a regulator of the cell cycle and cyclin D1 expression. Oncogene 42 15378006
2008 Structure of the yeast Pml1 splicing factor and its integration into the RES complex. Nucleic acids research 37 19033360
2019 Overexpression of miR-335 inhibits the migration and invasion of osteosarcoma by targeting SNIP1. International journal of biological macromolecules 27 30954590
2023 MKRN1 promotes colorectal cancer metastasis by activating the TGF-β signalling pathway through SNIP1 protein degradation. Journal of experimental & clinical cancer research : CR 25 37620897
2021 Optimization of gamma-aminobutyric acid production by Lactobacillus brevis PML1 in dairy sludge-based culture medium through response surface methodology. Food science & nutrition 21 34136196
2023 LncRNA BCAN-AS1 stabilizes c-Myc via N6-methyladenosine-mediated binding with SNIP1 to promote pancreatic cancer. Cell death and differentiation 19 37726400
2024 The PML1-WDR5 axis regulates H3K4me3 marks and promotes stemness of estrogen receptor-positive breast cancer. Cell death and differentiation 18 38627584
2002 Identification of SnIP1, a novel protein that interacts with SNF1-related protein kinase (SnRK1). Plant molecular biology 18 12008897
2020 The promyelocytic leukemia protein isoform PML1 is an oncoprotein and a direct target of the antioxidant sulforaphane (SFN). Biochimica et biophysica acta. Molecular cell research 17 32243901
2007 Regulation of ATR-dependent pathways by the FHA domain containing protein SNIP1. Oncogene 17 17260016
2017 Smad nuclear interacting protein 1 (SNIP1) inhibits intestinal inflammation through regulation of epithelial barrier function. Mucosal immunology 16 29426045
2023 The lncRNA H19/miR-29a-3p/SNIP1/c-myc regulatory axis is involved in pulmonary fibrosis induced by Nd2O3. Toxicological sciences : an official journal of the Society of Toxicology 13 37831906
2021 MiR-223 promotes pyroptosis of enteritis cells through activating NF-κB signalling pathway by targeting SNIP1 in inflammatory bowel disease. Autoimmunity 13 34151668
2023 MiR-138-5p suppresses the progression of lung cancer by targeting SNIP1. Thoracic cancer 12 36597175
2023 Curcumin reduces paclitaxel resistance in ovarian carcinoma cells by upregulating SNIP1 and inhibiting NFκB activity. Biochemical pharmacology 12 37146834
2024 LncRNA MSC-AS1 regulates SNIP1 SUMOylation-mediated EMT by binding to SENP1 to promote intestinal fibrosis in Crohn's disease. International journal of biological macromolecules 9 38309408
2023 SNIP1 reduces extracellular matrix degradation and inflammation via inhibiting the NF-κB signaling pathway in osteoarthritis. Archives of biochemistry and biophysics 9 37739115
2023 The non-ribosomal peptide synthetase-independent siderophore (NIS) rhizobactin produced by Caballeronia mineralivorans PML1(12) confers the ability to weather minerals. Applied and environmental microbiology 9 37800940
2021 A biallelic SNIP1 Amish founder variant causes a recognizable neurodevelopmental disorder. PLoS genetics 9 34570759
2015 Smad nuclear interacting protein, SNIP1, mediates the ecdysteroid signal transduction in red crayfish Procambarus clarkii. Journal of experimental zoology. Part A, Ecological genetics and physiology 7 25678477
2011 SNIP1: a new activator of HSE signaling pathway. Molecular and cellular biochemistry 7 22020748
2006 SNIP1: Myc's new helper in transcriptional activation. Molecular cell 6 17189184
2025 TET2 suppresses vascular calcification by forming an inhibitory complex with HDAC1/2 and SNIP1 independent of demethylation. The Journal of clinical investigation 5 40067382
2020 Modafinil ameliorated pancreatic injury and inflammation through upregulating SNIP1. General physiology and biophysics 5 32902407
2024 Acidification-based mineral weathering mechanism involves a glucose/methanol/choline oxidoreductase in Caballeronia mineralivorans PML1(12). Applied and environmental microbiology 4 39503492
2023 SNIP1 and PRC2 coordinate cell fates of neural progenitors during brain development. Nature communications 4 37553330
2024 The clinical utilization of SNIP1 and its pathophysiological mechanisms in disease. Heliyon 2 38304835
2023 The PML1-WDR5 axis regulates H3K4me3 marks and promotes stemness of estrogen receptor-positive breast cancer. Research square 2 37720048
2013 Silencing of the Smad nuclear interacting protein 1 (SNIP1) by siRNA inhibits proliferation and induces apoptosis in pituitary adenoma cells. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 1 23897559
2026 Phosphorylation of SF3B1 by CDK11 orchestrates spliceosome activation via SNIP1-dependent RES complex recruitment. Nature communications 0 41904131
2026 A PML1-CCL5-PI3K/MAPK feedback loop governs survival of endocrine-resistant breast cancer cells. Cell death and differentiation 0 42260104
2025 PML1-Mediated Feedforward Loop Through PI3K and MAPK Axes Drives Endocrine Resistance. bioRxiv : the preprint server for biology 0 40463196

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