Affinage

ATMIN

ATM interactor · UniProt O43313

Length
823 aa
Mass
88.3 kDa
Annotated
2026-06-09
37 papers in source corpus 21 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ATMIN (ASCIZ/ZNF822) is a dual-function protein that operates both as an ATM cofactor for non-DSB damage signaling and as a zinc-finger transcription factor controlling DYNLL1 expression (PMID:17525732, PMID:22167198). As an ATM partner, ATMIN binds ATM through a C-terminal motif and is required for ATM substrate phosphorylation in response to chloroquine, hypotonic stress, and oxidative stress, but not ionizing-radiation-induced DSBs; ATMIN and ATM reciprocally stabilize one another (PMID:17525732, PMID:20889973). Pathway choice between ATMIN- and NBS1-mediated ATM signaling is governed by direct competition for ATM binding: loss of one partner increases flux through the other, and double deficiency abrogates ATM signaling and causes profound radiosensitivity (PMID:17525732, PMID:23219553). After ionizing radiation, UBR5-mediated ubiquitination of ATMIN at K238 dissociates ATMIN from ATM to license MRN/NBS1-dependent signaling, and this is modulated upstream by PPARγ-promoted UBR5 activity (PMID:25092319, PMID:30699358). Independently, ATMIN binds the Dynll1 promoter via its zinc-finger domain and transcriptionally activates DYNLL1, while DYNLL1 protein binds multiple SQ/TQ motifs in ATMIN's activation domain to inhibit its activity, forming an autoregulatory negative feedback loop (PMID:22167198, PMID:21971545). Through this ASCIZ–DYNLL1 axis ATMIN drives DYNLL1-dependent 53BP1 oligomerization at DSBs to promote class switch recombination and PARP-inhibitor sensitivity of BRCA1-mutant tumors (PMID:30559443), supports B cell survival and development by suppressing the pro-apoptotic factor Bim and cooperating with MYC (PMID:22891272, PMID:26832406), sustains ciliogenesis (PMID:25294941), and enables TLR4/IL-1/CD40-dependent NF-κB activation (PMID:34543116).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2005 Medium

    Before ATMIN was linked to ATM, this work established it as a lesion-specific nuclear scaffold, showing it responds to a defined subset of DNA damage rather than DSBs.

    Evidence siRNA knockdown, focus-formation immunofluorescence, MLH1 epistasis and apoptosis assays after methylating damage

    PMID:15933716

    Open questions at the time
    • Molecular basis of methylation-lesion recognition undefined
    • Relationship to ATM signaling not yet established
    • Single lab, single readout class
  2. 2007 High

    Identified ATMIN as an ATM cofactor required for non-DSB ATM signaling and revealed NBS1 as a competing ATM partner, framing ATM activation as input-specific.

    Evidence Co-localization, reciprocal Co-IP, genetic deletion in murine fibroblasts and ATM substrate phosphorylation assays, including NBS1-impaired cells

    PMID:17525732 PMID:23219553

    Open questions at the time
    • Mechanism by which different stresses route to ATMIN vs NBS1 unresolved
    • Structural basis of the shared C-terminal ATM-binding motif not defined
  3. 2008 Medium

    Demonstrated that ASCIZ influences base-repair pathway choice in B cells, separating its role from direct homologous recombination control.

    Evidence Gene targeting in chicken DT40 cells, Ig gene conversion and MMS-sensitivity assays, polβ epistasis

    PMID:18433721

    Open questions at the time
    • Molecular mechanism linking ASCIZ to substrate availability unclear
    • Whether effect is transcriptional or scaffold-based not resolved
  4. 2010 High

    Established ATMIN as the conduit for ATM activation by oxidative stress, connecting it to DNA damage accumulation and senescence during aging.

    Evidence Constitutive and conditional KO mice, ATM/substrate phosphorylation, senescence and antioxidant-rescue assays, aged-brain immunohistochemistry

    PMID:20889973

    Open questions at the time
    • How oxidative stress is sensed upstream of ATMIN unknown
    • Physiological aging phenotype mechanism beyond DNA damage accumulation incomplete
  5. 2011 High

    Defined ATMIN's second identity as a zinc-finger transcription factor and revealed the autoregulatory ASCIZ–DYNLL1 feedback loop linking it to its product.

    Evidence ChIP, luciferase reporters with zinc-finger mutants, Co-IP, in vitro binding and multi-species deletion; plus Y2H/pepscan/NMR docking and live-cell imaging

    PMID:21971545 PMID:22167198

    Open questions at the time
    • Genome-wide target repertoire beyond DYNLL1 not mapped
    • How DYNLL1 binding mechanistically inhibits transcriptional activity not fully resolved
  6. 2011 High

    Connected ATMIN-dependent ATM signaling to adaptive immunity, showing it is required for V(D)J/class switch recombination and prevents lymphomagenic translocations.

    Evidence B cell-conditional Atmin knockout mice, ATM substrate phosphorylation, translocation analysis, lymphoma monitoring

    PMID:21575860

    Open questions at the time
    • Whether immune defect is via ATM cofactor or DYNLL1 transcriptional arm not separated here
    • Translocation mechanism details incomplete
  7. 2012 High

    Resolved ATM pathway selection genetically and placed ATMIN upstream of DYNLL1/Bim in B cell survival.

    Evidence atmin/nbs1 double-mutant epistasis with radiosensitivity assays; conditional KO with DYNLL1 ectopic rescue and Bim deletion epistasis

    PMID:22891272 PMID:23219553

    Open questions at the time
    • Switch determinant controlling ATMIN-vs-NBS1 flux still unknown
    • Direct DYNLL1 target genes beyond Bim regulation unmapped
  8. 2014 High

    Identified UBR5-mediated K238 ubiquitination as the molecular switch dissociating ATMIN from ATM after IR, and extended ATMIN's transcriptional function to ciliogenesis and Wnt/PCP signaling.

    Evidence Co-IP, in vitro ubiquitination, K238 mutagenesis, checkpoint/focus assays; conditional KO and rescue for cilia and Vangl2 genetic interaction for kidney/Wnt

    PMID:24852369 PMID:25092319 PMID:25294941

    Open questions at the time
    • Signal triggering UBR5 recruitment to ATMIN after IR not defined
    • Whether ciliary and Wnt phenotypes are entirely DYNLL1-dependent unresolved
  9. 2016 High

    Showed the ASCIZ–DYNLL1 axis is co-opted by MYC and is essential for survival of MYC-driven pre-neoplastic and malignant B cells, establishing therapeutic relevance.

    Evidence Conditional/constitutive deletion in Eμ-Myc lymphoma model, flow cytometry, apoptosis and survival analysis

    PMID:26832406

    Open questions at the time
    • Mechanism of ASCIZ-MYC synergy at the DYNLL1 promoter not detailed
    • Downstream effectors beyond DYNLL1 in this context not identified
  10. 2017 Medium

    Challenged the replication-stress ATM model by showing ASCIZ is dispensable for aphidicolin-induced ATM activation, leaving the role of ATMIN in replication-stress signaling unsettled.

    Evidence ATM substrate phosphorylation in ASCIZ-KO MEFs and human deleted lymphoma cells treated with aphidicolin

    PMID:28648892

    Open questions at the time
    • Directly contradicts the WRNIP1/PCNA replication-stress findings
    • Different damaging agents and cell systems may explain discrepancy
  11. 2018 High

    Provided the mechanistic link from ASCIZ-driven DYNLL1 to DSB repair, showing DYNLL1 promotes 53BP1 oligomerization governing class switch recombination and PARP-inhibitor response.

    Evidence Dynll1/Asciz deletion, 53BP1 binding-motif mutagenesis, oligomerization/Co-IP and CSR assays, in vivo PARPi treatment of BRCA1-mutant tumors

    PMID:30559443

    Open questions at the time
    • Whether ATMIN ATM-cofactor function contributes independently of DYNLL1 here unaddressed
    • Structural basis of 53BP1 oligomer assembly incomplete
  12. 2021 Medium

    Extended the ASCIZ–DYNLL1 axis to innate-type signaling, showing it is selectively required for TLR4/IL-1/CD40-dependent NF-κB activation.

    Evidence B-cell conditional Dynll1/Asciz KO, NF-κB reporters, IκBα phosphorylation/degradation assays, in vivo antibody responses

    PMID:34543116

    Open questions at the time
    • Molecular target of DYNLL1 upstream of IκBα unidentified
    • Why signaling is receptor-selective unexplained
  13. 2024 Medium

    Identified USP10 as a deubiquitinase stabilizing ATMIN and uncovered LCK as a transcriptional target in cancer, broadening ATMIN's transcriptional output and oncogenic roles.

    Evidence Mass spectrometry, Co-IP, ChIP-seq/RNA-seq, knockdown/overexpression, in vitro and in vivo proliferation/drug-sensitivity assays

    PMID:38321024

    Open questions at the time
    • Generality of LCK regulation beyond nasopharyngeal carcinoma unknown
    • Interplay between USP10 stabilization and UBR5 degradation not integrated

Open questions

Synthesis pass · forward-looking unresolved questions
  • How specific stress inputs are decoded to partition ATM signaling between ATMIN and NBS1, and the full genome-wide ATMIN transcriptional program beyond DYNLL1 and LCK, remain unresolved.
  • No structural model of the ATM–ATMIN interface
  • Conflicting data on replication-stress role unreconciled
  • Determinants linking upstream lesion type to UBR5-dependent dissociation unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0140110 transcription regulator activity 3 GO:0003677 DNA binding 2
Localization
GO:0005634 nucleus 3
Pathway
R-HSA-168256 Immune System 3 R-HSA-73894 DNA Repair 3 R-HSA-74160 Gene expression (Transcription) 2 R-HSA-8953897 Cellular responses to stimuli 1
Partners
ATMDYNLL1NBS1PARP1UBR5USP10WRNIP1

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 ATMIN interacts with ATM through a C-terminal motif (also present in NBS1), is required for ATM signaling induced by chloroquine and hypotonic stress (but not ionizing radiation-induced DSBs), and ATMIN and ATM mutually stabilize each other's protein levels. Co-localization, co-immunoprecipitation, genetic deletion in primary murine fibroblasts, ATM substrate phosphorylation assays The EMBO journal High 17525732
2007 NBS1 and ATMIN compete for binding to ATM: IR-induced complex disruption between ATMIN and ATM was attenuated in cells with impaired NBS1 function, suggesting NBS1 displaces ATMIN from ATM after DSBs. Co-immunoprecipitation in NBS1-impaired and wild-type cells after ionizing radiation The EMBO journal High 17525732 23219553
2012 NBS1 and ATMIN directly compete for ATM binding to control ATM signaling pathway choice: absence of ATMIN increases flux through the NBS1/IR pathway, and absence of NBS1 increases ATMIN-dependent ATM signaling; double deficiency completely abrogates ATM signaling and causes profound radiosensitivity. Genetic epistasis using atmin and nbs1 mutant mouse cells, ATM substrate phosphorylation assays, radiosensitivity assays Cell reports High 23219553
2014 UBR5 (E3 ubiquitin ligase) interacts with ATMIN and ubiquitinates ATMIN at lysine 238 in an IR-stimulated manner; this ubiquitination decreases ATMIN's interaction with ATM and promotes MRN-mediated (NBS1-dependent) ATM signaling after DNA damage. Mutation of ATMIN K238 prevents ATMIN dissociation from ATM and inhibits NBS1 foci formation, checkpoint activation, and increases radiosensitivity. Co-immunoprecipitation, in vitro ubiquitination assay, site-directed mutagenesis (K238), focus formation assays, checkpoint activation assays Proceedings of the National Academy of Sciences of the United States of America High 25092319
2015 Monoubiquitinated PCNA (a marker of stalled replication forks) interacts with ATMIN via WRNIP1, and RAD18 (E3 ligase for PCNA monoubiquitination), WRNIP1, and ATMIN are specifically required for ATM signaling and 53BP1 focus formation induced by replication stress but not by ionizing radiation. Co-immunoprecipitation, siRNA/genetic knockdown, focus formation assays, ATM substrate phosphorylation assays Oncogene Medium 26549024
2017 NEGATIVE RESULT: ASCIZ/ATMIN is dispensable for ATM activation and phosphorylation of KAP1, p53, and H2AX in response to the replication-blocking agent aphidicolin, in both immortalized and primary ASCIZ/ATMIN-deficient MEFs and human ASCIZ/ATMIN-deleted lymphoma cells. ATM substrate phosphorylation assays in ASCIZ/ATMIN knockout MEFs and human deleted lymphoma cells treated with aphidicolin DNA repair Medium 28648892
2005 ASCIZ (ATMIN) forms nuclear foci in response to DNA methylating agents (but not DSB-inducing agents), acts as a lesion-specific scaffold that recruits Rad51 and promotes Rad51 focus formation in response to base methylation damage in an MLH1-dependent manner; ASCIZ depletion dramatically increases apoptosis after methylating DNA damage. siRNA knockdown, immunofluorescence focus formation assays, epistasis with MLH1, apoptosis assays The EMBO journal Medium 15933716
2010 ATMIN is required for ATM signaling in response to oxidative stress: atmin-null MEFs show reduced ATM phosphorylation and substrate phosphorylation after acute oxidative stress, accumulate DNA damage and prematurely senesce at atmospheric oxygen, and this defect is rescued by antioxidant or physiological oxygen. Conditional neural ATMIN deletion impairs aging-induced ATM signaling and causes accumulation of DNA damage in the aging cortex. Conditional and constitutive genetic knockout, ATM/substrate phosphorylation assays, senescence assays, antioxidant rescue, immunohistochemistry in aged brain The Journal of biological chemistry High 20889973
2011 ASCIZ (ATMIN) directly binds the Dynll1 promoter via its Zn2+ finger domain and transcriptionally activates DYNLL1 expression; DYNLL1 protein in turn binds to ten sites in the ASCIZ transcriptional activation domain and inhibits ASCIZ transcriptional activity, forming a negative feedback loop that auto-regulates DYNLL1 levels. DYNLL1 levels are reduced ~10-fold in ASCIZ-deficient human, mouse, and chicken cells. Chromatin immunoprecipitation (ChIP), luciferase reporter assays with zinc-finger domain mutants, co-immunoprecipitation, in vitro binding assays, genetic deletion across three species The Journal of biological chemistry High 22167198
2011 DYNLL1 (LC8) binds to multiple SQ/TQ motifs in the C-terminal domain of ATMIN; co-expression of DYNLL1 and ATMIN mutually affects their intracellular localization, and DYNLL1 co-expression partly impedes DNA damage-induced ATMIN nuclear focus formation. Yeast two-hybrid, pepscan, gel filtration, NMR structure-based docking, live-cell fluorescence imaging of co-expressed fluorescent-tagged proteins Biochemical and biophysical research communications Medium 21971545
2011 ATMIN deficiency in B cells impairs ATM signaling and results in defective peripheral V(D)J rearrangement and class switch recombination, leading to chromosomal translocations involving the Igh and Igl loci and B cell lymphoma development. B cell-conditional Atmin knockout mice, ATM substrate phosphorylation assays, chromosomal translocation analysis, lymphoma monitoring Cancer cell High 21575860
2012 ASCIZ regulates B cell development by activating DYNLL1 expression; ASCIZ-deficient B cell precursors have highly reduced DYNLL1 levels, the B cell lymphopenia in ASCIZ-deficient mice can be fully suppressed by deletion of the pro-apoptotic DYNLL1 target Bim, or rescued by ectopic DYNLL1 expression, placing ASCIZ upstream of DYNLL1 and Bim in B cell survival. Conditional knockout mice, ectopic DYNLL1 expression rescue, Bim genetic deletion epistasis, flow cytometry of B cell populations The Journal of experimental medicine High 22891272
2014 ATMIN functions as a transcriptional regulator required for ciliogenesis primarily by controlling Dynll1 expression; depletion of ATMIN or DYNLL1 in cultured cells causes ciliary shortening and bulging similar to retrograde IFT mutants, and this is rescued by ectopic DYNLL1 or DYNLL2 expression. DYNLL1 and DYNLL2 localize to cilia in puncta consistent with IFT particles and physically interact with WDR34. Conditional mouse knockouts, siRNA depletion rescue with ectopic expression, immunofluorescence/confocal localization, co-immunoprecipitation (DYNLL1 with WDR34) Development (Cambridge, England) High 25294941
2014 Atmin is required for normal kidney morphogenesis; Atmin mutant kidneys exhibit altered cytoskeletal organization and modulation of Wnt signaling pathway molecules including β-catenin, Daam2, and Vangl2, and genetic interaction between Atmin and Vangl2 was demonstrated by intercross experiments, placing ATMIN in the non-canonical Wnt/PCP pathway. Atmin mutant mouse model, genetic intercross epistasis (Atmin × Vangl2), immunostaining, transcriptional analysis Human molecular genetics Medium 24852369
2016 ASCIZ (ATMIN) synergizes with MYC to transcriptionally activate DYNLL1 expression; deletion of Asciz or Dynll1 prevents abnormal pre-B cell expansion in pre-cancerous Eμ-Myc mice, potentiates MYC-induced apoptosis, and delays lymphoma development, establishing the ASCIZ-DYNLL1 axis as essential for survival of MYC-driven pre-neoplastic and malignant B cells. Conditional and constitutive genetic deletion in Eμ-Myc mouse lymphoma model, flow cytometry, apoptosis assays, survival analysis of tumor-bearing mice Cell reports High 26832406
2018 DYNLL1 promotes 53BP1 oligomerization and recruitment to DSB-associated chromatin, stimulated by its interaction with 53BP1. Deletion of Dynll1 or its transcriptional regulator Asciz, or mutation of DYNLL1 binding motifs in 53BP1, compromises class switch recombination and renders BRCA1-mutant cells and tumors resistant to PARP inhibitor treatment. Genetic deletion (Dynll1, Asciz), site-directed mutagenesis of DYNLL1 binding motifs in 53BP1, Co-IP/oligomerization assays, class switch recombination assays, in vivo PARP inhibitor treatment of BRCA1-mutant tumors Nature communications High 30559443
2019 PPARγ promotes UBR5 E3 ligase activity targeting ATMIN: PPARγ depletion increases ATMIN protein levels independent of transcription and suppresses DDR-induced ATM signaling; blocking ATMIN in this context restores ATM activation and DNA repair. In PAH patient PAECs, disrupted PPARγ-UBR5 interaction leads to heightened ATMIN expression and unresolved DNA damage. Proteomic/Co-IP interaction studies, siRNA knockdown, quantitative proteomics, ATM substrate phosphorylation assays, patient-derived cells Cell reports Medium 30699358
2021 ASCIZ (ATMIN) and DYNLL1 are required for TLR4-, IL-1-, and CD40-mediated NF-κB pathway activation in B cells and fibroblasts (but not for antigen receptor or TNF-α signaling); DYNLL1 acts upstream of IκBα phosphorylation and degradation in this signal-specific pathway. B-cell-specific conditional knockout of Dynll1 and Asciz, NF-κB reporter assays, IκBα phosphorylation/degradation assays, in vivo antibody response assays Molecular and cellular biology Medium 34543116
2008 ASCIZ deficiency in chicken DT40 B lymphocytes markedly increases Ig gene conversion rates, while ASCIZ overexpression reduces it below wild-type levels; ASCIZ loss suppresses the MMS hypersensitivity of polβ-deficient cells, indicating ASCIZ influences base repair pathway choice by reducing substrate availability for Ig gene conversion without directly controlling homologous recombination or abasic site formation. Gene targeting (knockout/overexpression) in chicken DT40 cells, Ig gene conversion assays, MMS sensitivity assays, epistasis with polβ deletion Biochemical and biophysical research communications Medium 18433721
2023 Inter-motif linker length and specific motif sequences in the ASCIZ transcriptional activation domain control binding affinity and compositional heterogeneity of multivalent ASCIZ:DYNLL1 (LC8) complexes; short linkers between strong and weak motifs yield stable but potentially off-register duplexes, while long linkers produce heterogeneous complexes, and negative-stain EM shows two-mers dominate rather than expected three-mers. Isothermal titration calorimetry, analytical ultracentrifugation, native mass spectrometry, negative-stain electron microscopy, systematic motif deactivation mutagenesis Biomolecules Medium 36979339
2024 USP10 deubiquitinase interacts with and stabilizes ATMIN protein; ATMIN transcriptionally activates LCK expression (confirmed by ChIP-seq), and the USP10-ATMIN-LCK axis promotes cell proliferation and docetaxel resistance in nasopharyngeal carcinoma. Mass spectrometry, Co-IP, ChIP-seq combined with RNA-seq, siRNA knockdown, overexpression, in vitro and in vivo proliferation/sensitivity assays Cell death & disease Medium 38321024
2021 ATMIN interacts with PARP1 (shown by co-immunoprecipitation) and acts on the Wnt signaling pathway via PARP1, influencing β-catenin/TCF4 binding affinity in MSI-high colorectal cancer; PARP1 inhibition decreases metastasis from ATMIN-knockdown cells. Co-immunoprecipitation, microarray/GSEA, PARP1 inhibitor treatment, in vivo metastasis model Annals of surgical oncology Low 34148137

Source papers

Stage 0 corpus · 37 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2018 The ASCIZ-DYNLL1 axis promotes 53BP1-dependent non-homologous end joining and PARP inhibitor sensitivity. Nature communications 87 30559443
2007 ATMIN defines an NBS1-independent pathway of ATM signalling. The EMBO journal 72 17525732
2019 PPARγ Interaction with UBR5/ATMIN Promotes DNA Repair to Maintain Endothelial Homeostasis. Cell reports 70 30699358
2014 UBR5-mediated ubiquitination of ATMIN is required for ionizing radiation-induced ATM signaling and function. Proceedings of the National Academy of Sciences of the United States of America 58 25092319
2011 ATM substrate Chk2-interacting Zn2+ finger (ASCIZ) Is a bi-functional transcriptional activator and feedback sensor in the regulation of dynein light chain (DYNLL1) expression. The Journal of biological chemistry 55 22167198
2010 The ATM cofactor ATMIN protects against oxidative stress and accumulation of DNA damage in the aging brain. The Journal of biological chemistry 52 20889973
2005 ASCIZ regulates lesion-specific Rad51 focus formation and apoptosis after methylating DNA damage. The EMBO journal 49 15933716
2014 ATMIN is a transcriptional regulator of both lung morphogenesis and ciliogenesis. Development (Cambridge, England) 39 25294941
2015 RAD18, WRNIP1 and ATMIN promote ATM signalling in response to replication stress. Oncogene 38 26549024
2012 Competition between NBS1 and ATMIN controls ATM signaling pathway choice. Cell reports 38 23219553
2012 The Zinc-finger protein ASCIZ regulates B cell development via DYNLL1 and Bim. The Journal of experimental medicine 35 22891272
2011 ATMIN is required for maintenance of genomic stability and suppression of B cell lymphoma. Cancer cell 33 21575860
2010 Dual functions of ASCIZ in the DNA base damage response and pulmonary organogenesis. PLoS genetics 33 20975950
2011 LC8 dynein light chain (DYNLL1) binds to the C-terminal domain of ATM-interacting protein (ATMIN/ASCIZ) and regulates its subcellular localization. Biochemical and biophysical research communications 31 21971545
2016 A Comprehensive Analysis of the Dynamic Response to Aphidicolin-Mediated Replication Stress Uncovers Targets for ATM and ATMIN. Cell reports 29 27149854
2016 The Transcription Factor ASCIZ and Its Target DYNLL1 Are Essential for the Development and Expansion of MYC-Driven B Cell Lymphoma. Cell reports 28 26832406
2014 ATMIN is required for the ATM-mediated signaling and recruitment of 53BP1 to DNA damage sites upon replication stress. DNA repair 28 25262557
2008 ATMINistrating ATM signalling: regulation of ATM by ATMIN. Cell cycle (Georgetown, Tex.) 27 19001856
2018 Atmin modulates Pkhd1 expression and may mediate Autosomal Recessive Polycystic Kidney Disease (ARPKD) through altered non-canonical Wnt/Planar Cell Polarity (PCP) signalling. Biochimica et biophysica acta. Molecular basis of disease 20 30414501
2016 Inactivation of the ATMIN/ATM pathway protects against glioblastoma formation. eLife 18 26984279
2016 Mechanisms and consequences of ATMIN repression in hypoxic conditions: roles for p53 and HIF-1. Scientific reports 16 26875667
2014 Atmin mediates kidney morphogenesis by modulating Wnt signaling. Human molecular genetics 13 24852369
2008 DNA damage response protein ASCIZ links base excision repair with immunoglobulin gene conversion. Biochemical and biophysical research communications 13 18433721
2019 ATMIN Is a Tumor Suppressor Gene in Lung Adenocarcinoma. Cancer research 12 31481498
2015 DNA Repair Cofactors ATMIN and NBS1 Are Required to Suppress T Cell Activation. PLoS genetics 12 26544571
2021 Involvement of ATMIN-DYNLL1-MRN axis in the progression and aggressiveness of serous ovarian cancer. Biochemical and biophysical research communications 10 34273621
2023 Linker Length Drives Heterogeneity of Multivalent Complexes of Hub Protein LC8 and Transcription Factor ASCIZ. Biomolecules 9 36979339
2017 ASCIZ/ATMIN is dispensable for ATM signaling in response to replication stress. DNA repair 9 28648892
2011 A breathtaking phenotype: unexpected roles of the DNA base damage response protein ASCIZ as a key regulator of early lung development. Cell cycle (Georgetown, Tex.) 9 21415597
2008 Mdt1/ASCIZ: a new DNA damage response protein family. Cell cycle (Georgetown, Tex.) 9 18728389
2023 CircMAN1A2 contributes to nasopharyngeal carcinoma progression via enhancing the ubiquitination of ATMIN through miR-135a-3p/UBR5 axis. Human cell 8 36626032
2021 ATMIN Suppresses Metastasis by Altering the WNT-Signaling Pathway via PARP1 in MSI-High Colorectal Cancer. Annals of surgical oncology 7 34148137
2024 Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma. Cell death & disease 6 38321024
2021 The ASCIZ-DYNLL1 Axis Is Essential for TLR4-Mediated Antibody Responses and NF-κB Pathway Activation. Molecular and cellular biology 6 34543116
2016 Perturbed hematopoiesis in mice lacking ATMIN. Blood 6 27581360
2016 Novel biomarkers in kidney disease: roles for cilia, Wnt signalling and ATMIN in polycystic kidney disease. Biochemical Society transactions 5 27913685
2022 ATMIN enhances invasion by altering PARP1 in MSS colorectal cancer. American journal of cancer research 0 36119811

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