Affinage

SPIN1

Protein spinster homolog 1 · UniProt Q9H2V7

Length
528 aa
Mass
56.6 kDa
Annotated
2026-06-10
38 papers in source corpus 17 papers cited in narrative 17 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SPIN1 (Spindlin1) is a multivalent histone-mark reader that functions as a chromatin-associated transcriptional co-regulator driving expression of proliferative and oncogenic gene programs (PMID:25749382, PMID:29168801). Its triple Tudor domain architecture recognizes methylated histone epitopes, with Tudor domain II engaging trimethyllysine peptides and the aromatic cage of the triple Tudor domain reading asymmetric dimethylarginine at H3R8 through electrostatically tunable CH3-π/cation-π interactions (PMID:31260300, PMID:38533580, PMID:39023428). Through these reader activities SPIN1 occupies chromatin to activate oncogenic targets: in cooperation with the transcription factor MAZ it enhances GDNF/RET signaling (PMID:25749382), and it binds H3K4me3 at the MDM2 promoter to activate MDM2 within a SPIN1-MDM2-p21-E2F1 positive feedback loop in gastric cancer (PMID:32767629). SPIN1 additionally controls the p53 axis post-transcriptionally by sequestering the ribosomal protein uL18 (RPL5) in the nucleolus, preventing uL18 from inhibiting MDM2 and thereby restraining p53 activation (PMID:29547122). Its N-terminal intrinsically disordered region (IDR) is central to several activities: it drives liquid-like phase separation that recruits the methyltransferase MLL1, enriches H3K4 methylation, and amplifies genome-wide chromatin binding at MAPK pathway genes (PMID:38777743), and it binds Poly-ADP-ribose to recruit SPIN1 to DNA double-strand breaks, where it promotes H3K9me3 accumulation, H3K9me3-Tip60 interaction, ATM activation, and homologous-recombination repair (PMID:39090319). SPIN1 forms a stable nucleosome-bound complex with WDR76 while recognizing H3K4me3 (PMID:39116123) and is regulated by cofactors including SPIN.DOC, which docks via its C-terminal domain to modulate SPIN1 chromatin localization and Wnt-repressive activity (PMID:30803761). SPIN1 activity is spatially gated during the oocyte-to-embryo transition by the SCMC component FILIA, which retains SPIN1 in the cytoplasm; loss of FILIA permits nuclear SPIN1 to compete with KDM5B for H3K4me3 and impair zygotic genome activation (PMID:40247146). Conditional Spin1 ablation in myoblast precursors causes severe sarcomere disorganization, necrosis, and lethality, establishing an essential developmental role through direct chromatin targets (PMID:29168801).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2015 High

    Established that SPIN1's oncogenic function depends on direct chromatin association, linking it to a transcription-factor partner and a defined oncogenic target rather than a vague nuclear role.

    Evidence ChIP-seq, transcriptomics, reader-domain mutagenesis, MAZ knockdown, and xenografts in liposarcoma cells

    PMID:25749382

    Open questions at the time
    • Did not resolve which histone mark drives MAZ-dependent recruitment
    • Generality of the GDNF/RET program beyond liposarcoma untested
  2. 2016 Medium

    Placed SPIN1 upstream of a canonical proliferation/survival pathway, broadening its functional output beyond direct transcription.

    Evidence SPIN1 knockdown/overexpression with Western blots of PI3K-Akt components and migration/invasion/chemoresistance assays in breast cancer cells and xenografts

    PMID:27171498

    Open questions at the time
    • Pathway placement via indirect miRNA-target approach
    • No demonstration of direct chromatin occupancy at PI3K-Akt genes
  3. 2017 High

    Demonstrated an essential in vivo developmental requirement and identified genome-wide direct targets in a non-cancer tissue.

    Evidence Conditional Spin1 knockout mice (Myf5-Cre), ChIP-seq in primary myoblasts, staged transcriptomics, and histology

    PMID:29168801

    Open questions at the time
    • Which reader activity drives myoblast target selection not dissected
    • Mechanistic link between chromatin targets and sarcomere phenotype incomplete
  4. 2018 High

    Revealed a transcription-independent route by which SPIN1 controls p53, through nucleolar sequestration of a ribosomal protein that otherwise inhibits MDM2.

    Evidence Reciprocal Co-IP, nucleolar fractionation, SPIN1 ablation, and genetic epistasis with uL18/uL5 depletion

    PMID:29547122

    Open questions at the time
    • Structural basis of SPIN1-uL18 binding unresolved
    • How nucleolar SPIN1 pool is partitioned from chromatin pool unclear
  5. 2019 High

    Defined SPIN1 as a druggable methyllysine reader by mapping inhibitor binding to a specific Tudor domain.

    Evidence Trimethyllysine peptide displacement assay, SPIN1-MS31 co-crystal structure, and cellular target engagement

    PMID:31260300

    Open questions at the time
    • Tudor domain II selectivity did not yet block all three reader pockets
    • Cellular phenotypic consequences of inhibition not fully characterized
  6. 2019 Medium

    Identified SPIN.DOC as a direct cofactor that tunes SPIN1 stability, chromatin localization, and a Wnt-repressive output.

    Evidence Co-IP, chromatin fractionation, TOPflash reporter assays, and C-terminal deletion mutagenesis

    PMID:30803761

    Open questions at the time
    • Single lab; no structural model of the SPIN.DOC-SPIN1 interface
    • Mechanism switching SPIN1 between activation and repression unresolved
  7. 2020 Medium

    Connected SPIN1 H3K4me3 reading to direct MDM2 promoter activation within a self-reinforcing transcriptional feedback loop.

    Evidence ChIP at the MDM2 promoter, E2F1-SPIN1 promoter luciferase reporter, and proliferation/cell-cycle assays in gastric cancer cells

    PMID:32767629

    Open questions at the time
    • Single lab; loop dynamics not quantitatively modeled
    • Relationship to the nucleolar uL18-MDM2 mechanism not integrated
  8. 2021 Medium

    Showed the SPIN1 cofactor Spindoc has a stage-specific essential role in spermatid development, distinguishing it from meiotic function.

    Evidence Two independent CRISPR/Cas9 Spindoc knockout mouse models with histological spermatid analysis

    PMID:34526015

    Open questions at the time
    • Whether the phenotype requires SPIN1 binding not directly tested
    • Molecular targets of the Spindoc-SPIN1 complex in spermatids unknown
  9. 2023 Medium

    Identified an upstream RNA-level control of SPIN1 abundance via alternative splicing, placing SPIN1 downstream of an RNA-binding regulator in cancer growth.

    Evidence RT-PCR splicing analysis, HNRNPK knockdown, intronic splicing enhancer mapping, and SPIN1 overexpression rescue

    PMID:36736887

    Open questions at the time
    • Single lab; in vivo relevance of the lncRNA isoform untested
    • How splicing choice is regulated across tissues unknown
  10. 2024 Medium

    Established that SPIN1's N-terminal IDR drives phase separation that recruits MLL1, locally enriches H3K4 methylation, and amplifies genome-wide chromatin binding.

    Evidence In vitro and cellular phase-separation assays with FRAP, SPIN1-MLL1 co-condensate assays, and IDR-dependent ChIP-seq

    PMID:38777743

    Open questions at the time
    • Single lab; physiological condensate concentration thresholds unclear
    • Whether condensation is required in vivo not tested
  11. 2024 High

    Defined a DNA-damage role: the same IDR binds PAR to recruit SPIN1 to double-strand breaks where it promotes H3K9me3-Tip60-ATM-driven homologous recombination.

    Evidence Laser micro-irradiation imaging, PAR binding assay, Co-IP, HR reporter, and ATM activation assays

    PMID:39090319

    Open questions at the time
    • How SPIN1 promotes H3K9me3 accumulation mechanistically unclear
    • Relationship between PAR-recruited and transcription-associated SPIN1 pools unresolved
  12. 2024 High

    Provided a structural model of SPIN1 in a stable complex by mapping the WDR76:SPIN1 nucleosome assembly and linking it to the DNA damage response.

    Evidence Serial capture affinity purification, cross-linking mass spectrometry, and Bayesian integrative structural modeling with H3K4me3 co-purification

    PMID:39116123

    Open questions at the time
    • Functional consequence of WDR76 binding for SPIN1 reader activity not dissected
    • Whether this complex overlaps with the PAR/HR pathway untested
  13. 2024 High

    Advanced selective chemical probes occupying a Tudor pocket and disrupting SPIN1-H3 binding in cells with oral bioavailability, enabling in vivo interrogation.

    Evidence SPIN1-compound 11 co-crystal, 38-target selectivity panel, NanoBRET cellular engagement, and mouse pharmacokinetics

    PMID:38533580

    Open questions at the time
    • In vivo efficacy against SPIN1-driven tumors not yet shown
    • Probe occupies a single Tudor domain, leaving other reader functions intact
  14. 2024 Medium

    Provided the physico-chemical basis for arginine-methyl recognition, explaining how H3R8me2a creates a new SPIN1 binding epitope.

    Evidence Quantitative binding with Tudor mutants, computational electrostatic (cation-π) analysis, and model peptide experiments

    PMID:39023428

    Open questions at the time
    • Single lab in vitro study
    • Cellular consequence of tuned H3R8me2a reading not tested
  15. 2024 Medium

    Mapped a competitive, X/Y-linked protein interaction network on SPIN1's third Tudor domain, implicating SPIN1 in genetic conflict between paralog families.

    Evidence Yeast protein-interaction assays, domain-deletion mapping, competition binding, and dimerization assays (preprint)

    PMID:bio_10.1101_2024.10.18.619120

    Open questions at the time
    • Preprint; interactions not validated in mammalian cells
    • Functional consequence of SLX/SLY competition unknown
  16. 2025 High

    Showed SPIN1 reader activity must be spatially restrained during the oocyte-to-embryo transition, identifying FILIA-mediated cytoplasmic retention as the gating mechanism.

    Evidence Co-IP, subcellular fractionation/immunofluorescence, FILIA knockout mice, embryo H3K4me3 ChIP, and KDM5B-competition rescue

    PMID:40247146

    Open questions at the time
    • Molecular basis of FILIA-SPIN1 cytoplasmic anchoring unresolved
    • Whether other SPIN1 nuclear functions are similarly gated unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SPIN1's distinct functional pools — chromatin reader, nucleolar uL18 sequestration, PAR-recruited DSB repair factor, and phase-separated condensate hub — are coordinated and partitioned within a single cell remains unresolved.
  • No unified model reconciling the nucleolar, chromatin, and DNA-damage pools
  • Post-translational or partner-driven switching between these functions uncharacterized
  • Integration of cytoplasmic gating (FILIA) with somatic-cell functions untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0042393 histone binding 6 GO:0140110 transcription regulator activity 3 GO:0098772 molecular function regulator activity 2 GO:0140313 molecular sequestering activity 2
Localization
GO:0005634 nucleus 4 GO:0000228 nuclear chromosome 2 GO:0005730 nucleolus 1 GO:0005829 cytosol 1
Pathway
R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1643685 Disease 3 R-HSA-4839726 Chromatin organization 2 R-HSA-73894 DNA Repair 2
Partners
FILIAHNRNPKKAT5MAZMLL1RPL5SPIN.DOCWDR76
Complex memberships
SPIN.DOC-SPIN1 complexWDR76:SPIN1 nucleosome complex

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2015 SPIN1 directly enhances expression of GDNF (an activator of the RET signaling pathway) in cooperation with the transcription factor MAZ by binding to chromatin; a reader-domain mutation that interferes with chromatin binding reduces liposarcoma cell proliferation and survival, demonstrating that chromatin association is required for SPIN1's oncogenic function. Genome-wide chromatin binding (ChIP-seq), transcriptome analysis, knockdown of SPIN1/MAZ, active-site mutagenesis of the reader domain, xenograft mouse models Oncotarget High 25749382
2018 SPIN1 sequesters the ribosomal protein uL18 (RPL5) in the nucleolus, preventing uL18 from interacting with MDM2 and thereby relieving uL18-mediated inhibition of MDM2 ubiquitin ligase activity toward p53. SPIN1 depletion increases free uL18 and uL5, which are required for SPIN1-depletion-induced p53 activation. Co-immunoprecipitation (SPIN1–uL18 binding), nucleolar fractionation, knockdown/ablation of SPIN1, epistasis with uL18/uL5 depletion, cell growth/apoptosis assays eLife High 29547122
2019 SPIN1 is a methyllysine reader protein; a potent and selective fragment-like inhibitor (MS31/compound 3) was developed that binds specifically to tudor domain II of SPIN1, blocking binding of trimethyllysine-containing peptides. Crystal structure of the SPIN1–MS31 complex confirmed tudor domain II selectivity. Biochemical binding assay (trimethyllysine peptide displacement), crystal structure determination (SPIN1–inhibitor complex), cellular target engagement assay Journal of medicinal chemistry High 31260300
2024 SPIN1 co-crystal structure with compound 11 confirmed that inhibitors occupy one of the three Tudor domains of SPIN1. A SPIN1-selective inhibitor (MS8535/compound 18) disrupts SPIN1–H3 interactions in cells in a concentration-dependent manner and shows oral bioavailability in mice. Co-crystal structure (SPIN1–compound 11), selectivity panel (38 epigenetic targets), cellular NanoBRET/proximity assay, pharmacokinetic assessment in mice Journal of medicinal chemistry High 38533580
2024 CH3–π interactions between methyl groups of asymmetric dimethylarginine (H3R8me2a) and aromatic cage residues in the SPIN1 triple Tudor domain are electrostatically tunable (cation-π character), providing a mechanistic explanation for how arginine methylation creates a new binding epitope recognized by SPIN1. Quantitative binding assays with Tudor domain mutants, computational electrostatic analysis (cation-π), model peptide experiments (NMR/fluorescence) Journal of the American Chemical Society Medium 39023428
2024 SPIN1 is recruited to DNA double-strand break lesions via its N-terminal intrinsically disordered region (IDR) that binds Poly-ADP-ribose (PAR). At damage sites, SPIN1 promotes H3K9me3 accumulation and enhances the interaction between H3K9me3 and Tip60, thereby activating ATM and homologous recombination (HR) repair. Laser micro-irradiation/live-cell imaging (recruitment assay), PAR binding assay, Co-IP (SPIN1–Tip60–H3K9me3), knockdown with DSB repair readouts (γH2AX, HR reporter), ATM activation assay EMBO reports High 39090319
2024 SPIN1's N-terminal IDR drives formation of liquid-like phase-separated condensates that recruit the histone methyltransferase MLL1, enrich H3K4 methylation marks, facilitate SPIN1 binding to H3K4me3, and enhance SPIN1 genome-wide chromatin binding at MAPK pathway genes. Phase separation assay in vitro and in cells (fluorescence microscopy, FRAP), Co-condensate assay (SPIN1–MLL1), ChIP-seq (genome-wide chromatin occupancy with and without IDR), H3K4me3 ChIP Journal of molecular cell biology Medium 38777743
2024 SPIN1 facilitates MDM2-mediated ubiquitination and degradation of FOXO3a, leading to upregulation of FOXM1, which in turn promotes DNA double-strand break repair and NSCLC radioresistance. Knockdown/overexpression with cell proliferation, cell-cycle (G2/M), clonogenic, and DSB-repair assays; rescue experiments with FOXM1 restoration; ubiquitination assay for FOXO3a Cell death & disease Medium 39548064
2024 SPIN1 forms a stable complex with WDR76 while recognizing H3K4me3; cross-linking mass spectrometry and integrative structural modeling (Bayesian IMP) built a model of WDR76:SPIN1 bound to the nucleosome. Interaction network analysis of co-purifying proteins implicated this complex in the DNA damage response. Serial capture affinity purification (SCAP), cross-linking mass spectrometry, Bayesian Integrative Modeling Platform (IMP), co-purification of H3K4me3, fluorescence microscopy Proceedings of the National Academy of Sciences of the United States of America High 39116123
2025 The SCMC component FILIA directly interacts with SPIN1 and retains it in the cytoplasm. Loss of FILIA causes residual SPIN1 to translocate to the nucleus, where it impairs H3K4me3 reprogramming and zygotic genome activation by competing with KDM5B for binding to H3K4me3. Co-immunoprecipitation (FILIA–SPIN1), subcellular fractionation/immunofluorescence (cytoplasmic vs. nuclear SPIN1), embryo live imaging, H3K4me3 ChIP in embryos, FILIA knockout mice, H3K4me3–SPIN1 interaction inhibition rescue experiment Nature structural & molecular biology High 40247146
2020 SPIN1 sustains gastric cancer cell proliferation by binding to H3K4me3 at the MDM2 promoter region, activating MDM2 expression. E2F1 directly binds the SPIN1 promoter and activates SPIN1 transcription, forming a SPIN1–MDM2–p21–E2F1 positive feedback loop. ChIP (SPIN1 on MDM2 promoter H3K4me3), luciferase reporter (E2F1 on SPIN1 promoter), knockdown/overexpression with cell-cycle and proliferation assays Molecular oncology Medium 32767629
2017 Conditional ablation of Spin1 in murine myoblast precursors (Myf5-Cre) causes severe sarcomere disorganization, necrosis, and lethality, with genome-wide Spin1 chromatin occupancy revealing direct target genes including deregulated bHLH transcription factor networks, aberrant titin-associated proteins, and abnormal glycogen metabolism. Conditional Spin1 knockout mice (Myf5-Cre), ChIP-seq (primary myoblasts), transcriptome analysis at multiple embryonic stages, histology Cell death & disease High 29168801
2019 SPIN.DOC (Spindlin docking protein) directly interacts with SPIN1 via its C-terminal domain; SPIN.DOC overexpression increases SPIN1 expression and chromatin localization. SPIN.DOC knockdown slightly destabilizes SPIN1 without altering its chromatin localization. The SPIN.DOC–SPIN1 complex acts as a transcriptional repressor of Wnt signaling; a C-terminal deletion mutant of SPIN.DOC that cannot bind SPIN1 instead activates Wnt signaling. shRNA knockdown, Co-IP (SPIN.DOC–SPIN1), chromatin fractionation, TOPflash Wnt reporter assay, C-terminal deletion mutagenesis Biochemical and biophysical research communications Medium 30803761
2021 Spindoc (the Spin1-interacting cofactor that enhances Spin1 binding to histone marks) is dispensable for meiotic division but is specifically required for haploid spermatid development in mice, as shown by CRISPR/Cas9 knockout models. CRISPR/Cas9 Spindoc knockout mice (two independent models), histological and spermatid developmental analysis Reproductive biology and endocrinology : RB&E Medium 34526015
2023 HNRNPK promotes SPIN1 exon 4 inclusion by interacting with an intronic splicing enhancer in intron 4 of SPIN1 pre-mRNA; exon 4 skipping generates a long non-coding RNA isoform that leads to reduced SPIN1 protein. SPIN1 overexpression partially rescues the growth inhibition caused by HNRNPK knockdown, placing SPIN1 downstream of HNRNPK in an epigenetic cancer regulatory pathway. RNA splicing analysis (RT-PCR), HNRNPK knockdown, SPIN1 overexpression rescue, RNABP–RNA interaction mapping (intronic splicing enhancer), cell growth/cell-cycle assays Journal of molecular biology Medium 36736887
2024 SLXL1 and SLX (X-linked) compete with SLY1 and SLY2 (Y-linked) for binding to the third Tudor domain of SPIN1 in a dose-dependent, protein-family-specific manner; SLY1 and SLY2 form homo- and heterodimers, indicating competition between multimeric complexes. Positive selection maps to the interaction domains. Yeast-based protein–protein interaction assay, domain-deletion mapping (N-terminal and Tudor domain III of SPIN1), competition binding assay, dimerization assay bioRxivpreprint Medium bio_10.1101_2024.10.18.619120
2016 SPIN1 activates the PI3K-Akt signaling pathway in breast cancer cells; knockdown of SPIN1 suppresses PIK3CA, AKT, CREB1, and BCL2, and inhibiting SPIN1 reduces cell migration, invasion, and resistance to chemotherapy. miRNA overexpression/inhibition, SPIN1 knockdown/overexpression, Western blot for PI3K-Akt pathway components, in vitro and in vivo (xenograft) functional assays The Journal of pathology Medium 27171498

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2016 Suppression of SPIN1-mediated PI3K-Akt pathway by miR-489 increases chemosensitivity in breast cancer. The Journal of pathology 103 27171498
2008 SPIN1, a K homology domain protein negatively regulated and ubiquitinated by the E3 ubiquitin ligase SPL11, is involved in flowering time control in rice. The Plant cell 73 18586868
2017 Suppressive role exerted by microRNA-29b-1-5p in triple negative breast cancer through SPIN1 regulation. Oncotarget 55 28423652
2018 SPIN1 promotes tumorigenesis by blocking the uL18 (universal large ribosomal subunit protein 18)-MDM2-p53 pathway in human cancer. eLife 51 29547122
2015 The histone code reader SPIN1 controls RET signaling in liposarcoma. Oncotarget 51 25749382
2018 SPIN1, negatively regulated by miR-148/152, enhances Adriamycin resistance via upregulating drug metabolizing enzymes and transporter in breast cancer. Journal of experimental & clinical cancer research : CR 50 29743122
2017 miR-489 inhibits proliferation, cell cycle progression and induces apoptosis of glioma cells via targeting SPIN1-mediated PI3K/AKT pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 49 28666210
2019 LINC00473/miR-374a-5p regulates esophageal squamous cell carcinoma via targeting SPIN1 to weaken the effect of radiotherapy. Journal of cellular biochemistry 39 31017716
2018 miR-409 Inhibits Human Non-Small-Cell Lung Cancer Progression by Directly Targeting SPIN1. Molecular therapy. Nucleic acids 34 30290307
2019 Discovery of a Potent and Selective Fragment-like Inhibitor of Methyllysine Reader Protein Spindlin 1 (SPIN1). Journal of medicinal chemistry 30 31260300
2020 Circ_0086720 knockdown strengthens the radiosensitivity of non-small cell lung cancer via mediating the miR-375/SPIN1 axis. Neoplasma 28 32940043
2018 MiR-1271 as a tumor suppressor in breast cancer proliferation and progression via targeting SPIN1. European review for medical and pharmacological sciences 25 29771421
2020 E2F1-activated SPIN1 promotes tumor growth via a MDM2-p21-E2F1 feedback loop in gastric cancer. Molecular oncology 23 32767629
2018 SPIN1 is a proto-oncogene and SPIN3 is a tumor suppressor in human seminoma. Oncotarget 22 30197756
2021 Histone code reader SPIN1 is a promising target of cancer therapy. Biochimie 18 34492335
2019 Spindlin docking protein (SPIN.DOC) interaction with SPIN1 (a histone code reader) regulates Wnt signaling. Biochemical and biophysical research communications 17 30803761
2021 The microRNA-381(miR-381)/Spindlin1(SPIN1) axis contributes to cell proliferation and invasion of colorectal cancer cells by regulating the Wnt/β-catenin pathway. Bioengineered 14 34753384
2017 The histone code reader Spin1 controls skeletal muscle development. Cell death & disease 13 29168801
2023 Epigenetic Control of Cancer Cell Proliferation and Cell Cycle Progression by HNRNPK via Promoting Exon 4 Inclusion of Histone Code Reader SPIN1. Journal of molecular biology 12 36736887
2020 Long Non-Coding RNA SNHG14 Regulates SPIN1 Expression to Accelerate Tumor Progression in Non-Small Cell Lung Cancer by Sponging miR-382-5p. Cancer management and research 12 33061605
2019 MicroRNA-489 promotes cardiomyocyte apoptosis induced by myocardial ischemia-reperfusion injury through inhibiting SPIN1. European review for medical and pharmacological sciences 9 31378911
2025 The subcortical maternal complex safeguards mouse oocyte-to-embryo transition by preventing nuclear entry of SPIN1. Nature structural & molecular biology 8 40247146
2024 An integrated structural model of the DNA damage-responsive H3K4me3 binding WDR76:SPIN1 complex with the nucleosome. Proceedings of the National Academy of Sciences of the United States of America 8 39116123
2024 Exosome-transported of circ_0081069 induces SPIN1 production by binding to miR-195-5p to inhibit radiosensitivity in esophageal squamous cell carcinoma. Journal of biochemical and molecular toxicology 6 38348706
2024 Contribution of Electrostatic CH3-π Interactions to Recognition of Histone Asymmetric Dimethylarginine by the SPIN1 Triple Tudor Domain. Journal of the American Chemical Society 6 39023428
2024 SPIN1 accelerates tumorigenesis and confers radioresistance in non-small cell lung cancer by orchestrating the FOXO3a/FOXM1 axis. Cell death & disease 6 39548064
2022 Circ_0001686 knockdown suppresses tumorigenesis and enhances radiosensitivity in esophagus cancer through regulating miR-876-5p/SPIN1 axis. Pathology, research and practice 6 36459832
2021 The Spin1 interactor, Spindoc, is dispensable for meiotic division, but essential for haploid spermatid development in mice. Reproductive biology and endocrinology : RB&E 6 34526015
2022 Hsa_circ_0000129 drives tumor growth via sequestering miR-485-3p and upregulating SPIN1 in breast cancer. Journal of biochemical and molecular toxicology 4 36426627
2024 SPIN1 facilitates chemoresistance and HR repair by promoting Tip60 binding to H3K9me3. EMBO reports 3 39090319
2022 The role of Heisenberg spin exchange and the quantum Zeno effect in the spin-selective reaction between spin-1/2 and spin-1 particles. The Journal of chemical physics 3 35963733
2024 Discovery of a Potent, Selective, and Cell-Active SPIN1 Inhibitor. Journal of medicinal chemistry 2 38533580
2024 Phase separation of SPIN1 through its IDR facilitates histone methylation readout and tumorigenesis. Journal of molecular cell biology 2 38777743
2018 A spin-1 representation for dual-funnel energy landscapes. The Journal of chemical physics 2 30037251
2014 RBS1, an RNA binding protein, interacts with SPIN1 and is involved in flowering time control in rice. PloS one 2 24498057
2001 Dynamics of a spin-1 Ising system in the neighborhood of equilibrium states. Physical review. E, Statistical, nonlinear, and soft matter physics 2 11497646
2025 Molecular mechanism of interactions of SPIN1 with novel inhibitors through molecular docking and molecular dynamics simulations. SAR and QSAR in environmental research 0 39989297
2023 Serial Capture Affinity Purification and Integrated Structural Modeling of the H3K4me3 Binding and DNA Damage Related WDR76:SPIN1 Complex. bioRxiv : the preprint server for biology 0 36778327

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