Affinage

DCLRE1A

DNA cross-link repair 1A protein · UniProt Q6PJP8

Length
1040 aa
Mass
116.4 kDa
Annotated
2026-06-09
44 papers in source corpus 17 papers cited in narrative 17 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

DCLRE1A (hSNM1A, the functional homolog of yeast Pso2) is a nuclear 5'-exonuclease that operates in DNA interstrand crosslink (ICL) repair through a pathway parallel to and genetically distinct from the Fanconi anemia pathway (PMID:10848582, PMID:18006388, PMID:18180189). Its catalytic activity is a single-strand 5'-exonuclease that processes either DNA or RNA, requires a 5'-phosphate, acts on the enzyme as a monomer, and depends on a conserved aspartate in its metallo-β-lactamase domain (PMID:17804464); the broader SNM1 family combines this exonuclease mode with structure-specific endonuclease activity, including DNA hairpin opening required for repair of breaks with closed hairpin ends (PMID:22102580). At ICL lesions DCLRE1A is recruited and stimulated by partner proteins: direct binding of the CSB (ERCC6) winged-helix domain to the SNM1A nuclease core enhances resection through crosslinks and increases affinity for damaged DNA [PMID:bio_10.1101_2024.09.05.611390], and RecQ4-family helicases stimulate Pso2 translesion nuclease activity through site-specific ICLs (PMID:32371399). Beyond crosslink repair, DCLRE1A localizes to nuclear foci, redistributes after ionizing radiation and crosslinking agents, physically associates with 53BP1, and colocalizes with Mre11 (PMID:12446782), and together with 53BP1 it co-immunoprecipitates with the anaphase-promoting complex to enforce an early mitotic stress checkpoint distinct from the spindle assembly checkpoint (PMID:15542852). The protein additionally shapes repair outcomes at repetitive sequences, recognizing nuclease-generated structures and interacting with SLX4 and POLI [PMID:bio_10.1101_2025.11.18.689026], and undergoes dual nuclear/mitochondrial targeting governed by competing localization signals and SUMO modification (PMID:35482533, PMID:37649278). In mice Snm1 functions as a tumor suppressor with a role in immunity (PMID:16260620).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2000 High

    Established that DCLRE1A has a direct, conserved role in interstrand crosslink repair rather than merely correlating with crosslink sensitivity.

    Evidence Mouse SNM1 knockout ES cells and mice sensitive to mitomycin C, rescued by human SNM1 cDNA complementation

    PMID:10848582

    Open questions at the time
    • Did not define the biochemical activity underlying repair
    • Did not place SNM1 relative to other ICL repair pathways
  2. 2002 High

    Connected DCLRE1A to damage-response foci and a candidate protein partner, framing it as part of an organized DNA damage response.

    Evidence Immunofluorescence showing IR/crosslink-induced foci, co-IP with 53BP1, colocalization with Mre11, focus-formation domain mapping

    PMID:12446782

    Open questions at the time
    • Functional consequence of the 53BP1 interaction not established
    • No catalytic activity demonstrated
  3. 2004 High

    Revealed a cell-cycle role distinct from DNA repair, linking DCLRE1A to mitotic checkpoint control via the APC.

    Evidence Snm1-deficient MEFs with mitotic checkpoint defects, co-IP of Snm1 and 53BP1 with APC/cyclosome components

    PMID:15542852

    Open questions at the time
    • Mechanism by which Snm1 targets the APC unresolved
    • Relationship between nuclease activity and checkpoint role unclear
  4. 2007 High

    Defined the core biochemical activity: DCLRE1A is a metallo-β-lactamase-dependent 5'-exonuclease and a functional homolog of yeast Pso2.

    Evidence Recombinant protein exonuclease assays, active-site aspartate mutagenesis, substrate requirement analysis, yeast pso2 complementation across multiple phenotypes

    PMID:17804464 PMID:18006388

    Open questions at the time
    • How a 5'-exonuclease processes a crosslinked duplex not explained
    • Substrate engagement at ICLs not directly tested
  5. 2008 High

    Placed DCLRE1A in an ICL repair pathway operating in parallel to, and genetically separable from, the Fanconi anemia pathway.

    Evidence siRNA depletion in human fibroblasts, additive MMC sensitivity with FA cells, intact FANCD2 mono-ubiquitination

    PMID:18180189

    Open questions at the time
    • Molecular branch point between the two pathways not defined
    • Order of action relative to incision/recruitment unknown
  6. 2005 High

    Demonstrated an organism-level consequence of DCLRE1A loss as a tumor suppressor with immune functions.

    Evidence Snm1 knockout mice with accelerated tumorigenesis and infection susceptibility, Trp53 double-knockout epistasis, immune profiling

    PMID:16260620

    Open questions at the time
    • Mechanistic basis for tumor suppression not linked to specific nuclease substrate
    • Immune phenotype mechanism unresolved
  7. 2011 High

    Expanded the catalytic repertoire of the family to include structure-specific endonuclease/hairpin-opening activity needed in vivo.

    Evidence In vitro nuclease assays on multiple substrate structures and in vivo hairpin-end break repair assay in yeast Pso2

    PMID:22102580

    Open questions at the time
    • Hairpin-opening activity shown for yeast Pso2, human SNM1A direct confirmation absent
    • Structural basis of endo- vs exonuclease switching not defined here
  8. 2021 Medium

    Provided a structural rationale for substrate selectivity and endo/exo activity through a 5'-phosphate binding pocket.

    Evidence X-ray product-state structure of SNM1B/Apollo with bound nucleotides, pocket mutagenesis, nuclease assays on modified substrates

    PMID:34387694

    Open questions at the time
    • Direct structure is of SNM1B with inference to SNM1A
    • No SNM1A-specific structure with ICL substrate
  9. 2020 High

    Identified a helicase partner that stimulates DCLRE1A nuclease activity to enable translesion processing through ICLs.

    Evidence Genetic epistasis, gel-based and smFRET nuclease assays, domain-mapped interaction of Hrq1 (RecQ4) with Pso2

    PMID:32371399

    Open questions at the time
    • Shown in yeast; human SNM1A/RecQ4 stimulation not directly demonstrated
    • In vivo contribution of stimulation to repair outcome unquantified
  10. 2022 High

    Established dual nuclear/mitochondrial targeting under competitive control of MTS and NLS signals, extending DCLRE1A function to mitochondria.

    Evidence Subcellular fractionation, imaging, and systematic mutagenesis of MTS/NLS in yeast Pso2

    PMID:35482533

    Open questions at the time
    • Mitochondrial substrate/function not defined
    • Conservation of dual targeting in human SNM1A not shown
  11. 2023 High

    Showed SUMOylation regulates damage-dependent mitochondrial partitioning of the nuclease, coupling a PTM to organelle-specific genome protection.

    Evidence In vivo SUMOylation assays, K97R/K575R mutants, E3 ligase genetics, mitochondrial DNA damage NGS in yeast Pso2

    PMID:37649278

    Open questions at the time
    • Agent specificity (MMS vs ICL) mechanism unexplained
    • Human SNM1A SUMOylation not demonstrated
  12. 2024 Medium

    Identified CSB as a direct recruiter and activator of SNM1A at ICLs, defining a mechanism for damage-site engagement and resection enhancement.

    Evidence Domain-level interaction mapping (CSB winged-helix to SNM1A nuclease core), in vitro ICL resection assays, single-molecule studies (preprint)

    PMID:bio_10.1101_2024.09.05.611390

    Open questions at the time
    • Preprint, not yet peer-reviewed
    • Cellular requirement of CSB for SNM1A recruitment not confirmed in vivo
  13. 2025 Medium

    Implicated DCLRE1A as an effector of repeat instability outcomes through interactions with SLX4 and POLI at nuclease-generated structures.

    Evidence Genome-wide CRISPRi screen, DNA binding assays, co-IP/interaction assays, editing outcome analysis (preprint)

    PMID:bio_10.1101_2025.11.18.689026

    Open questions at the time
    • Preprint, not yet peer-reviewed
    • Direct nature and stoichiometry of SLX4/POLI interactions not fully resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How human DCLRE1A coordinates its exonuclease and endonuclease activities, partner recruitment, and dual organelle targeting into a unified ICL repair mechanism distinct from the FA pathway remains unresolved.
  • No human SNM1A structure bound to an ICL substrate
  • In vivo human confirmation of mitochondrial targeting and SUMO regulation absent
  • Mechanistic link between nuclease activity and mitotic checkpoint function unestablished

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140097 catalytic activity, acting on DNA 4 GO:0003677 DNA binding 2 GO:0016787 hydrolase activity 2
Localization
GO:0005634 nucleus 3 GO:0005739 mitochondrion 2
Pathway
R-HSA-73894 DNA Repair 3 R-HSA-1640170 Cell Cycle 1
Partners
ERCC6POLISLX4TP53BP1

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 Human SNM1 (DCLRE1A) is a nuclear protein involved in DNA interstrand cross-link (ICL) repair; mouse SNM1-/- embryonic stem cells and mice are sensitive to mitomycin C, and this sensitivity is complemented by transfection of human SNM1 cDNA, establishing a direct role in ICL repair. Gene knockout in mouse ES cells and mice, complementation by human SNM1 cDNA transfection, mitomycin C sensitivity assay Molecular and cellular biology High 10848582
2002 Human SNM1 (DCLRE1A) localizes to the cell nucleus in distinct patterns (diffuse, foci, or nuclear bodies), redistributes to increased foci after ionizing radiation or interstrand crosslinking agent exposure, physically associates with 53BP1 (confirmed by coimmunoprecipitation), and colocalizes with Mre11 foci after ionizing radiation. A ~220 amino acid region of hSNM1 is sufficient for focus formation when attached to a nuclear localization signal. Indirect immunofluorescence, coimmunoprecipitation, domain mapping with nuclear localization signal constructs Molecular and cellular biology High 12446782
2002 hSNM1 translation is mediated by an internal ribosome entry site (IRES) in the 5' UTR that generally suppresses translation but upregulates it during mitosis, suggesting a cell-cycle-regulated mitotic function. Bicistronic construct assays to demonstrate IRES activity, cell-cycle synchronization DNA repair Medium 12509242
2004 Mammalian SNM1 functions in an early mitotic stress checkpoint distinct from the spindle assembly checkpoint; Snm1-deficient mouse embryonic fibroblasts exposed to spindle poisons show elevated micronucleus formation, decreased mitotic delay, failure to arrest prior to chromosome condensation, supernumerary centrosomes, and decreased viability. Both Snm1 and 53BP1 coimmunoprecipitate with components of the anaphase-promoting complex (APC/cyclosome), suggesting Snm1 negatively targets the APC before chromosome condensation. Snm1-deficient MEFs, spindle poison treatment, micronucleus assay, coimmunoprecipitation with APC components Molecular and cellular biology High 15542852
2007 Recombinant hSNM1A (DCLRE1A) is a 5'-exonuclease; ectopic expression of hSNM1A (but not SNM1B/Apollo or Artemis) suppresses yeast pso2 mutant sensitivity to crosslinking agents, rescues the DSB repair defect during cross-link processing, and partially rescues spontaneous intrachromosomal recombination defects, establishing hSNM1A as a functional homolog of yeast Pso2. Recombinant protein exonuclease assay, yeast complementation (suppression of pso2 sensitivity), DSB repair assay, intrachromosomal recombination assay DNA repair High 18006388
2007 hSNM1 (DCLRE1A) protein is a single-strand 5'-exonuclease that utilizes either DNA or RNA substrates, requires a 5'-phosphate moiety, shows very little activity on double-strand substrates, functions as a monomer, and requires the conserved beta-lactamase domain for activity (site-directed mutagenesis of a conserved aspartate inactivates the exonuclease). Recombinant protein overproduction in insect cells, in vitro exonuclease assays, site-directed mutagenesis Nucleic acids research High 17804464
2008 siRNA depletion of hSNM1 in human fibroblasts increases sensitivity to mitomycin C (ICL agent) as measured by cell survival and chromosome radial formation, and this sensitivity is additive with that of Fanconi anemia (FA) cells. Depletion of hSNM1 does not disturb FANCD2 mono-ubiquitination, indicating hSNM1 acts in a pathway parallel to and distinct from the FA pathway for ICL repair. siRNA depletion, cell survival assay, chromosome radial formation assay, FANCD2 ubiquitination western blot, epistasis with FA cell lines Molecular genetics and metabolism High 18180189
2005 Snm1-deficient mice exhibit accelerated tumorigenesis and susceptibility to bacterial infections, and crossing with Trp53 null mice increases mortality and restricts tumor types to lymphomas. Snm1 functions as a tumor suppressor in mice and has a role in immunity, distinct from T- and B-cell development or immunoglobulin class switching defects. Snm1 knockout mice, survival analysis, tumor pathology, Trp53 double knockout epistasis, immune cell profiling Molecular and cellular biology High 16260620
2011 Pso2 (yeast ortholog of SNM1A/DCLRE1A) is a structure-specific DNA hairpin opening endonuclease in addition to its known 5'-exonuclease activity; this hairpin-opening activity is required in vivo for repair of chromosomal breaks with closed hairpin ends. In vitro nuclease assays on multiple DNA substrate structures, in vivo genetic assay for hairpin-end chromosomal break repair in yeast Nucleic acids research High 22102580
2020 The Hrq1 helicase (RecQ4 subfamily) physically interacts with Pso2 (yeast ortholog of SNM1A/DCLRE1A) through their N-terminal domains and stimulates Pso2 nuclease activity, including translesion nuclease activity through site-specific ICLs in vitro; this stimulation requires Hrq1 catalytic activity and is specific to eukaryotic RecQ4 subfamily helicases. Genetic epistasis, in vitro nuclease assays (gel-based and smFRET), biochemical interaction mapping, domain analysis The Journal of biological chemistry High 32371399
2021 A structure of SNM1B/Apollo with two nucleotides bound to its active site reveals a 5' phosphate binding pocket that is important for catalysis and is a key determinant of endo- versus exonuclease activity across the SNM1 family including SNM1A; base modifications planar to the nucleobase are accommodated by the open active site architecture, while axial lesions are not well tolerated. X-ray crystallography (product-state structure), mutagenesis of phosphate-binding pocket residues, in vitro nuclease assays on modified substrates Nucleic acids research Medium 34387694
2022 Yeast Pso2 (ortholog of DCLRE1A/SNM1A) is dual-localized to both the nucleus and mitochondria; it contains one mitochondrial targeting sequence (MTS) and two nuclear localization signals (NLS1 and NLS2), with MTS essential for mitochondrial import and either NLS sufficient for nuclear import. Genotoxic agents enhance mitochondrial abundance of Pso2. Ablation of MTS abrogates mitochondrial import and raises nuclear levels, while disruption of both NLS motifs blocks nuclear import and enhances mitochondrial translocation, establishing competitive regulation between MTS and NLS. Subcellular fractionation, fluorescence imaging, mutational analysis of MTS and NLS sequences, in vitro and in vivo localization assays G3 (Bethesda, Md.) High 35482533
2023 Yeast Pso2 undergoes SUMOylation on residues K97 and K575 (catalyzed by Siz1 and Siz2 SUMO E3 ligases, with Siz1 dominant) specifically in response to methyl methanesulfonate (MMS) but not ICL-forming agents; SUMOylation markedly increases Pso2 abundance in mitochondria without affecting nuclear translocation, and SUMOylation-defective mutants (K97R/K575R) fail to translocate to mitochondria after MMS treatment and fail to suppress MMS-induced mitochondrial DNA damage. In vivo SUMOylation assays, site-directed mutagenesis of SUMO consensus sites, subcellular fractionation, genetic analysis of SUMO E3 ligase mutants, next-generation sequencing of mitochondrial DNA damage Molecular microbiology High 37649278
2013 Pso2 (yeast ortholog of DCLRE1A) is phosphorylated by the Sak1 kinase in vitro, coimmunoprecipitates with Sak1 after DNA damage (8-MOP+UVA treatment), and Sak1 interacts with the C-terminal β-CASP domain of Pso2 in two-hybrid assays; epistasis analysis shows SAK1 and PSO2 act in the same ICL repair pathway, while PSO2 and RAD52/RAD50/XRS2 act epistatically, and PSO2 and MRE11 act in distinct repair pathways on the same substrate. Yeast two-hybrid screen, in vitro kinase assay, coimmunoprecipitation, genetic epistasis with DNA damaging agents Journal of photochemistry and photobiology. B, Biology Medium 24362320
2025 DCLRE1A (human SNM1A) was identified via CRISPRi screen as a key effector of CAG repeat contraction following Cas12a-induced staggered cuts within repeat tracts; DCLRE1A recognizes and binds structures generated by Cas12a, interacts with SLX4 to promote pure contractions, and interacts with POLI to generate inverted repeats via template switching mechanisms. CRISPRi genome-wide screen, DNA binding assays, co-immunoprecipitation/interaction assays, editing outcome analysis bioRxivpreprint Medium bio_10.1101_2025.11.18.689026
2024 CSB (Cockayne Syndrome B/ERCC6) directly interacts with SNM1A (DCLRE1A) through a specific interaction between the winged-helix domain of CSB and the nuclease core of SNM1A; CSB enhances SNM1A resection through ICLs, increases SNM1A affinity for damaged DNA substrates, and alters substrate conformation to enhance ICL processing. CSB was observed preferentially as a dimer when colocalized with SNM1A at ICLs. Biochemical interaction mapping (domain-level), in vitro nuclease resection assays through ICLs, single-molecule studies on site-specific ICL substrates bioRxivpreprint Medium bio_10.1101_2024.09.05.611390
1999 Overexpression of SNM1 cDNA (human homolog, alias KIAA0086) in CHO cells does not render them more resistant to DNA crosslinking agents (mafosfamide, melphalan, mitomycin C), indicating that overexpression of SNM1 alone is not sufficient to confer ICL resistance in this cellular context. Transfection of human SNM1 cDNA into CHO cells, cell survival assay with crosslinking agents Anticancer research Low 10470107

Source papers

Stage 0 corpus · 44 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 A founder mutation in Artemis, an SNM1-like protein, causes SCID in Athabascan-speaking Native Americans. Journal of immunology (Baltimore, Md. : 1950) 130 12055248
2000 Disruption of mouse SNM1 causes increased sensitivity to the DNA interstrand cross-linking agent mitomycin C. Molecular and cellular biology 110 10848582
2005 DNA interstrand cross-link repair in the Saccharomyces cerevisiae cell cycle: overlapping roles for PSO2 (SNM1) with MutS factors and EXO1 during S phase. Molecular and cellular biology 64 15743825
2005 The yeast Snm1 protein is a DNA 5'-exonuclease. DNA repair 60 15590324
2003 The beta-lactamase motif in Snm1 is required for repair of DNA double-strand breaks caused by interstrand crosslinks in S. cerevisiae. DNA repair 52 12509272
2007 Human SNM1A suppresses the DNA repair defects of yeast pso2 mutants. DNA repair 50 18006388
1996 Regulation of SNM1, an inducible Saccharomyces cerevisiae gene required for repair of DNA cross-links. Molecular & general genetics : MGG 43 8628215
2010 The SNM1/Pso2 family of ICL repair nucleases: from yeast to man. Environmental and molecular mutagenesis 42 20175117
2007 The hSNM1 protein is a DNA 5'-exonuclease. Nucleic acids research 42 17804464
2024 Deucravacitinib in moderate-to-severe plaque psoriasis: Pooled safety and tolerability over 52 weeks from two phase 3 trials (POETYK PSO-1 and PSO-2). Journal of the European Academy of Dermatology and Venereology : JEADV 40 38451052
2012 Components of a Fanconi-like pathway control Pso2-independent DNA interstrand crosslink repair in yeast. PLoS genetics 38 22912599
2002 hSnm1 colocalizes and physically associates with 53BP1 before and after DNA damage. Molecular and cellular biology 38 12446782
2000 Saccharomyces cerevisiae lacking Snm1, Rev3 or Rad51 have a normal S-phase but arrest permanently in G2 after cisplatin treatment. Mutation research 37 10980408
2010 The multifunctional SNM1 gene family: not just nucleases. Future oncology (London, England) 36 20528238
1999 Mutagenesis of SNM1, which encodes a protein component of the yeast RNase MRP, reveals a role for this ribonucleoprotein endoribonuclease in plasmid segregation. Molecular and cellular biology 36 10523674
2005 The eukaryotic Pso2/Snm1/Artemis proteins and their function as genomic and cellular caretakers. Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas 34 15761611
2005 Snm1-deficient mice exhibit accelerated tumorigenesis and susceptibility to infection. Molecular and cellular biology 31 16260620
2004 Deficiency in SNM1 abolishes an early mitotic checkpoint induced by spindle stress. Molecular and cellular biology 31 15542852
2002 Translation of hSNM1 is mediated by an internal ribosome entry site that upregulates expression during mitosis. DNA repair 27 12509242
1995 Rescue of the fission yeast snRNA synthesis mutant snm1 by overexpression of the double-strand-specific Pac1 ribonuclease. Molecular & general genetics : MGG 27 7616961
2011 Pso2 (SNM1) is a DNA structure-specific endonuclease. Nucleic acids research 25 22102580
2013 The conserved Fanconi anemia nuclease Fan1 and the SUMO E3 ligase Pli1 act in two novel Pso2-independent pathways of DNA interstrand crosslink repair in yeast. DNA repair 23 24192486
1989 Molecular cloning of SNM1, a yeast gene responsible for a specific step in the repair of cross-linked DNA. Molecular & general genetics : MGG 23 2550766
1992 Molecular structure of the DNA cross-link repair gene SNM1 (PSO2) of the yeast Saccharomyces cerevisiae. Molecular & general genetics : MGG 22 1736091
2025 Deucravacitinib in plaque psoriasis: Four-year safety and efficacy results from the Phase 3 POETYK PSO-1, PSO-2 and long-term extension trials. Journal of the European Academy of Dermatology and Venereology : JEADV 21 40045918
2008 Mammalian SNM1 is required for genome stability. Molecular genetics and metabolism 21 18180189
2020 The yeast Hrq1 helicase stimulates Pso2 translesion nuclease activity and thereby promotes DNA interstrand crosslink repair. The Journal of biological chemistry 18 32371399
2008 Unique and overlapping functions of the Exo1, Mre11 and Pso2 nucleases in DNA repair. DNA repair 18 18295552
1994 A single amino acid change in SNM1-encoded protein leads to thermoconditional deficiency for DNA cross-link repair in Saccharomyces cerevisiae. Mutation research 14 7526204
2021 A phosphate binding pocket is a key determinant of exo- versus endo-nucleolytic activity in the SNM1 nuclease family. Nucleic acids research 12 34387694
1998 Genomic organization of a potential human DNA-crosslink repair gene, KIAA0086. Mutation research 11 9806498
2010 DNA repair mutant pso2 of Saccharomyces cerevisiae is sensitive to intracellular acetaldehyde accumulated by disulfiram-mediated inhibition of acetaldehyde dehydrogenase. Genetics and molecular research : GMR 9 20082270
2013 New features on Pso2 protein family in DNA interstrand cross-link repair and in the maintenance of genomic integrity in Saccharomyces cerevisiae. Fungal genetics and biology : FG & B 8 24076078
2007 Further characterization of the role of Pso2 in the repair of DNA interstrand cross-link-associated double-strand breaks in Saccharomyces cerevisiae. Neoplasma 8 17447848
2015 Unravelling the role of SNM1 in the DNA repair system of Trypanosoma brucei. Molecular microbiology 7 25689597
2011 The role of SNM1 family nucleases in etoposide-induced apoptosis. Biochemical and biophysical research communications 7 21683065
2023 DCLRE1A Contributes to DNA Damage Repair and Apoptosis in Age-Related Cataracts by Regulating the lncRNA/miRNA/mRNA Axis. Current eye research 6 37503815
2024 Deucravacitinib Improves Patient-Reported Outcomes in Patients with Moderate to Severe Psoriasis: Results from the Phase 3 Randomized POETYK PSO-1 and PSO-2 Trials. Dermatology and therapy 5 39080153
2013 Sak1 kinase interacts with Pso2 nuclease in response to DNA damage induced by interstrand crosslink-inducing agents in Saccharomyces cerevisiae. Journal of photochemistry and photobiology. B, Biology 5 24362320
1999 Overexpression of cDNA encoding FANCC, SPHAR, MPG, SNM1 or HA 3611 does not render CHO cells more resistant to DNA crosslinking agents. Anticancer research 5 10470107
2023 SUMOylation of yeast Pso2 enhances its translocation and accumulation in the mitochondria and suppresses methyl methanesulfonate-induced mitochondrial DNA damage. Molecular microbiology 3 37649278
2023 Structure and Function of SNM1 Family Nucleases. Advances in experimental medicine and biology 2 35708844
2022 Dual targeting of Saccharomyces cerevisiae Pso2 to mitochondria and the nucleus, and its functional relevance in the repair of DNA interstrand crosslinks. G3 (Bethesda, Md.) 2 35482533
2026 A novel and thermostable cyclomaltodextrin glucanotransferase from Anoxybacillus rupiensis PSO2 isolated from Yumthang hot spring: cloning and functional characterisation. Enzyme and microbial technology 0 41830721

Missed literature

Know a paper Affinage missed for DCLRE1A? Flag it for the maintainers and the community.

No submissions yet.