Affinage

CNOT2

CCR4-NOT transcription complex subunit 2 · UniProt Q9NZN8

Length
540 aa
Mass
59.7 kDa
Annotated
2026-06-09
36 papers in source corpus 17 papers cited in narrative 16 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

CNOT2 (yeast NOT2/CDC36) is a core structural and regulatory subunit of the evolutionarily conserved CCR4-NOT complex, a megadalton machine that couples transcriptional repression to cytoplasmic mRNA deadenylation (PMID:7926748, PMID:10490603, PMID:21299754). It was first defined in yeast as a general negative regulator of TATA-dependent RNA Pol II transcription that associates with NOT1/CDC39 in a discrete nuclear complex (PMID:7926748), and structural work resolved how it works: NOT2 wraps around the C-terminal HEAT-repeat scaffold of NOT1 and dimerizes with NOT5 through Sm-fold-like Not-box domains, forming a ternary 'Not module' whose composite surface binds RNA (PMID:10490603, PMID:24121231). This architecture is essential for complex integrity—the NOT2 N-terminus is required to maintain the ~1.9 MDa complex and NOT5 association (PMID:12215412), and in human cells CNOT2 depletion fragments the complex, abolishes CNOT6L-associated deadenylase activity, suppresses P-body formation, and triggers ER-stress-associated apoptosis (PMID:21299754). CNOT2 also acts directly in transcriptional repression: its conserved C-terminal Not-Box represses promoter-targeted reporters in an HDAC-dependent manner by recruiting the SMRT/NCoR–HDAC3 co-repressor complex (PMID:14707134, PMID:16712523). The complex's deadenylase output is dynamically controlled by post-translational modification, as osmotic-stress-activated MK2 phosphorylates CNOT2 to reduce CCR4-NOT deadenylase activity (PMID:35129087). Through these mRNA-regulatory activities CNOT2 has been linked to maintenance of ESC pluripotency by repressing trophectoderm factors such as Cdx2 (PMID:22367759), to adipogenic differentiation via interaction with PPARγ (PMID:26584287), to ATG5-dependent autophagic degradation of p62/SQSTM1 (PMID:28537904), and to dengue virus replication by accelerating deadenylase-mediated decay of JAK1 and STAT1 mRNAs (PMID:31155293).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1990 High

    Established the earliest functional role for NOT2/CDC36 as a negative regulator within a signaling pathway, before its molecular activity was known.

    Evidence Genetic epistasis with STE mutants and pheromone-inducible reporters in temperature-sensitive yeast mutants

    PMID:2099190 PMID:2111445

    Open questions at the time
    • Did not define the biochemical activity of CDC36
    • Connection between mating-response repression and later transcriptional/mRNA roles unresolved
  2. 1994 High

    Defined NOT2 as a general negative transcriptional regulator physically associated with NOT1 in a discrete complex, distinguishing it from other known repression machineries.

    Evidence Allele-specific suppressor screens, yeast two-hybrid, co-fractionation, and reporter assays in yeast

    PMID:7926748

    Open questions at the time
    • Mechanism of repression not defined
    • Did not connect transcriptional role to mRNA decay
  3. 1999 High

    Placed NOT2 in a defined module of the CCR4-NOT complex by mapping its interaction with the NOT1 C-terminus and its NOT5 partner, separate from the CCR4/CAF1 enzymatic subcomplex.

    Evidence Co-fractionation, co-IP, and deletion mapping with genetic interaction analysis in yeast

    PMID:10490603

    Open questions at the time
    • Structural basis of NOT1/NOT2/NOT5 contacts not resolved
    • Functional consequence of the module for enzymatic activity not tested
  4. 2002 High

    Showed the NOT2 N-terminus is required for overall complex integrity, identifying it as a structural anchor of the megadalton assembly.

    Evidence Site-directed mutagenesis (L9P, G31R), co-fractionation, and co-IP in yeast

    PMID:12215412

    Open questions at the time
    • Did not resolve atomic contacts
    • ADA2/SAGA contact significance unclear
  5. 2004 Medium

    Demonstrated that the human CNOT2 Not-Box is itself a transferable repression domain dependent on HDAC activity, extending the repression function to mammals.

    Evidence Gal4-fusion promoter-targeting reporter assays with Not-Box mutagenesis and TSA pharmacology in human cells

    PMID:14707134

    Open questions at the time
    • Did not identify the recruited HDAC complex
    • Single lab, reporter-based
  6. 2006 Medium

    Identified the SMRT/NCoR–HDAC3 co-repressor as the effector recruited by the CNOT2 Not-Box, explaining the TSA sensitivity of repression.

    Evidence Reciprocal co-IP, co-expression of co-repressor subunits, and reporter repression assays with Not-Box deletions

    PMID:16712523

    Open questions at the time
    • Native promoter targets not identified
    • Single lab
  7. 2011 High

    Established that in human cells CNOT2 is structurally required for CCR4-NOT integrity and deadenylase activity, directly linking complex assembly to enzymatic and cellular outputs.

    Evidence siRNA knockdown with sucrose gradient fractionation, deadenylase assays, P-body imaging, and apoptosis flow cytometry

    PMID:21299754

    Open questions at the time
    • Specific mRNA targets destabilized not enumerated
    • Mechanism linking complex loss to ER stress/apoptosis unclear
  8. 2013 High

    Resolved the atomic architecture of the Not module, showing NOT2/NOT5 wrap NOT1 via Sm-fold-like Not boxes and form a composite RNA-binding surface.

    Evidence 2.8 Å X-ray crystallography of the yeast Not1/Not2/Not5 module, in vitro poly(U) binding, structure-guided mutagenesis with in vivo growth assays

    PMID:24121231

    Open questions at the time
    • RNA-binding specificity in vivo not defined
    • Human complex structure not solved here
  9. 2021 High

    Showed CCR4-NOT deadenylase activity is dynamically tuned by stress-induced phosphorylation of CNOT2, establishing post-translational control of mRNA decay.

    Evidence MS phospho-mapping with phosphomimetic/non-phosphorylatable rescue, poly(A) length and in vitro deadenylase assays under osmotic stress

    PMID:35129087

    Open questions at the time
    • Structural basis of phospho-induced activity loss unresolved
    • Breadth of stress-regulated mRNA targets unknown
  10. 2017 Medium

    Connected CNOT2 to a cellular catabolic program by showing it promotes ATG5-dependent autophagic degradation of p62/SQSTM1.

    Evidence Knockdown/overexpression in ATG5 KO MEFs, ubiquitination assays, co-IP with PB1-domain mapping, and autophagic flux/LC3 imaging

    PMID:28537904

    Open questions at the time
    • Whether the effect requires deadenylase activity not established
    • Single lab
  11. 2012 Medium

    Extended CNOT2's developmental relevance by showing the CNOT1/2/3 module maintains pluripotency by repressing trophectoderm transcription factors.

    Evidence siRNA/shRNA in mouse and human ESCs with differentiation phenotyping, epistasis, and co-IP

    PMID:22367759

    Open questions at the time
    • Whether repression is transcriptional or mRNA-decay-mediated not resolved
    • Direct target mRNAs not mapped
  12. 2015 Medium

    Implicated CNOT2 in adipogenesis through a physical interaction with PPARγ.

    Evidence Co-IP, immunofluorescence, and siRNA loss-of-function in 3T3-L1 preadipocytes with differentiation readouts

    PMID:26584287

    Open questions at the time
    • Direct vs indirect interaction with PPARγ unresolved
    • Single lab
  13. 2019 Medium

    Demonstrated CNOT2 facilitates dengue replication by accelerating deadenylase-mediated decay of antiviral JAK1 and STAT1 mRNAs.

    Evidence RNAi screen, siRNA knockdown with mRNA stability qRT-PCR, co-IP with CNOT6/6L and CNOT7/8, and viral replication assays

    PMID:31155293

    Open questions at the time
    • Direct binding of CNOT2 to target mRNAs not shown
    • Single lab
  14. 2026 Low

    Reported CNOT2 interactions with oncogenic effectors (STAT3/c-Myc and VEGF) in cancer cells, suggesting roles in tumor metabolism and angiogenesis.

    Evidence Co-IP, knockdown/overexpression rescue, and functional assays in HCC and HeLa cells

    PMID:41629418 PMID:42045595

    Open questions at the time
    • Single co-IP studies without reciprocal/structural validation
    • Direct vs indirect interactions undefined
    • Not independently confirmed

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CNOT2's distinct activities—structural scaffolding, Not-Box-mediated transcriptional repression, and deadenylase regulation—are coordinated across its many biological contexts remains unresolved.
  • Whether transcriptional and mRNA-decay functions are mechanistically coupled is unknown
  • Genome-wide direct mRNA target set of CNOT2-containing complex not defined
  • No human Not-module structure in the timeline

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 3 GO:0140110 transcription regulator activity 3 GO:0098772 molecular function regulator activity 2 GO:0003723 RNA binding 1
Localization
GO:0005634 nucleus 2 GO:0005829 cytosol 1
Pathway
R-HSA-74160 Gene expression (Transcription) 3 R-HSA-8953854 Metabolism of RNA 2
Complex memberships
CCR4-NOT complexNot module (NOT1-NOT2-NOT5)SMRT/NCoR-HDAC3 co-repressor complex

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1994 NOT1 (CDC39) and NOT2 (CDC36) are nuclear proteins that associate in a discrete ~500 kDa complex, act as general negative regulators of transcription preferentially affecting TC-dependent (TATA element-dependent) transcription, and their function is distinct from CYC8/TUP1, nucleosome-mediated repression, and SPT4/5/6-mediated chromatin effects. Allele-specific suppression, two-hybrid interaction, and biochemical co-fractionation established these relationships. Allele-specific suppressor screens, yeast two-hybrid, biochemical co-fractionation, transcriptional reporter assays Genes & development High 7926748
1990 CDC36 (NOT2) acts as a negative element in the yeast mating pheromone response pathway; epistasis analysis with STE gene mutations placed CDC36 function at or upstream of the transducing G protein (Gα subunit level), required to block pathway activation in the absence of pheromone. Genetic epistasis analysis, pheromone-inducible reporter (FUS1) assays, temperature-sensitive mutant analysis Cell regulation High 2099190 2111445
1999 NOT2 physically associates with the C-terminal region (residues 1490–2108) of NOT1 in the CCR4-NOT complex; NOT2 and NOT5 interact with each other independently of CAF1, NOT3, and NOT4, placing them in a physically and functionally distinct module (CCR4–CAF1–NOT1–(NOT2, NOT5)) from the CCR4/CAF1 sub-complex. Loss of NOT2 does not disrupt CCR4–CAF1–NOT1 interactions. Biochemical co-fractionation, co-immunoprecipitation, deletion mapping, genetic interaction analysis Molecular and cellular biology High 10490603
2002 The N-terminus of NOT2 is required for stability of the 1.9 MDa CCR4-NOT complex and for NOT5 association; the not2::L9P mutation causes complete loss of the complex and increased NOT5–NOT2 interaction, while not2-4 (G31R) destabilizes the complex less severely. A separate region of NOT2 contacts ADA2 (a SAGA component), but disruption of the NOT2–ADA2 interaction does not necessarily affect CCR4-NOT complex integrity. Biochemical co-fractionation, co-immunoprecipitation, site-directed mutagenesis, yeast genetic analysis Journal of molecular biology High 12215412
2004 The CNOT2 subunit of the human CCR4-NOT complex acts as a direct transcriptional repressor when targeted to a promoter. The major repression activity resides in the conserved Not-Box motif at the C-terminus of CNOT2, and this repression is sensitive to the histone deacetylase inhibitor trichostatin A (TSA), implying involvement of HDAC activity. Promoter-targeting (Gal4-fusion) transient transfection reporter assays in human cells, Not-Box deletion and mutagenesis The Journal of biological chemistry Medium 14707134
2006 CNOT2-mediated transcriptional repression involves recruitment of the SMRT/NCoR–HDAC3 co-repressor complex; CNOT2 physically interacts with multiple subunits of this complex, and coexpression of SMRT or NCoR with HDAC3 (or HDAC5/6) augments CNOT2-dependent repression. The Not-Box of CNOT2 mediates both the repressive function and the physical interaction with this co-repressor complex. Co-immunoprecipitation, reporter gene repression assays, co-expression of SMRT/NCoR-HDAC3 subunits, Not-Box deletion analysis The Biochemical journal Medium 16712523
2013 Crystal structure of the yeast Not module (Not1 C-terminal arm + Not2 + Not5) resolved at 2.8 Å shows: Not1 is a HEAT-repeat scaffold; Not2 and Not5 have extended regions wrapping around Not1 and form Not box domains that dimerize via a noncanonical surface resembling Sm folds; the ternary complex forms a composite surface that binds poly(U) RNA in vitro, with the primary RNA-binding site at the Not5 Not box. Disruption of interactions within the ternary complex causes severe growth defects in vivo. X-ray crystallography (2.8 Å), in vitro RNA-binding assay, structure-guided mutagenesis with in vivo growth assays Nature structural & molecular biology High 24121231
2011 CNOT2 depletion by siRNA in human cells destabilizes the CCR4-NOT complex (forming a smaller sub-complex), reduces deadenylase activity of the CNOT6L-containing complex, suppresses P-body formation, and induces ER-stress-associated, caspase-dependent apoptosis. These data establish CNOT2 as structurally required for CCR4-NOT complex integrity and enzymatic deadenylase activity. siRNA knockdown, sucrose gradient fractionation, deadenylase activity assay, fluorescence microscopy (P-bodies), RT-qPCR, flow cytometry (apoptosis) Genes to cells High 21299754
2005 The caspase-processed kinase domain of CDK11 (CDK11p46) directly interacts with NOT2 via the NOT domain in the C-terminal part of NOT2. Both proteins co-localize predominantly in the nucleus. NOT2 is not phosphorylated by CDK11p46, indicating the interaction is not a kinase–substrate relationship. Yeast two-hybrid screening, in vitro binding assay, co-immunoprecipitation in human cells, co-localization by fluorescence microscopy Biochemical and biophysical research communications Medium 16039607
2012 Cnot1, Cnot2, and Cnot3 act together as a protein complex in mouse and human ESCs to maintain pluripotency and inhibit extraembryonic (trophectoderm and primitive endoderm) differentiation, specifically repressing early TE transcription factors such as Cdx2. Genetic analysis indicated this function is independent of known self-renewal pathways or core transcription factors (Oct4/Sox2/Nanog). siRNA/shRNA knockdown in mouse and human ESCs, gene expression analysis, genetic epistasis, immunofluorescence, co-IP to establish complex Stem cells Medium 22367759
2015 CNOT2 promotes adipogenic differentiation of 3T3-L1 preadipocytes; it physically interacts with PPARγ (but not C/EBPα) by co-immunoprecipitation, and CNOT2 depletion reverses activation of PPARγ and C/EBPα and prevents inhibition of GSK3α/β and β-catenin during differentiation. siRNA knockdown, co-immunoprecipitation, immunofluorescence co-localization, Western blot, Oil Red O staining Cellular physiology and biochemistry Medium 26584287
2017 CNOT2 acts as a negative regulator of ATG5-dependent autophagy; CNOT2 depletion causes p62/SQSTM1 accumulation and impairs autophagic flux. Conversely, CNOT2 overexpression promotes ubiquitination and degradation of p62/SQSTM1 in an ATG5-dependent manner (degradation detected in ATG5+/+ but not ATG5-/- MEF cells). CNOT2 co-localizes and co-immunoprecipitates with p62/SQSTM1, and interaction requires the PB1 domain of p62. siRNA/shRNA knockdown and overexpression, ATG5 knockout MEF cells, ubiquitination assay, co-immunoprecipitation, LC3 puncta imaging, autophagic flux assay Oncotarget Medium 28537904
2019 CNOT2 facilitates dengue virus replication by negatively regulating the IFN-independent non-canonical JAK/STAT pathway; mechanistically, CNOT2 accelerates mRNA decay of JAK1 and STAT1 through interaction with CNOT6/6L and CNOT7/8 deadenylases. CNOT2 knockdown enhances JAK-STAT antiviral signaling and reduces DENV RNA replication and protein synthesis. RNAi screen, siRNA knockdown, qRT-PCR for mRNA stability, co-immunoprecipitation (CNOT2 with deadenylase subunits), viral replication assays Biochemical and biophysical research communications Medium 31155293
2021 Osmotic stress induces MAPKAPK-2 (MK2)-dependent phosphorylation of CNOT2. Phosphomimetic CNOT2 (Ser→Glu) cannot rescue deadenylation defects or stress sensitivity in CNOT2-depleted cells, whereas wild-type and non-phosphorylatable CNOT2 can. The CCR4-NOT complex containing phosphomimetic CNOT2 has reduced deadenylase activity. This demonstrates that post-translational phosphorylation of CNOT2 by MK2 regulates CCR4-NOT deadenylase activity. Phosphorylation mapping by mass spectrometry, phosphomimetic/non-phosphorylatable mutant rescue assays, poly(A) tail length assays, in vitro deadenylase activity assay, stress-induced apoptosis assay RNA biology High 35129087
2026 CNOT2 physically interacts with STAT3 and c-Myc by co-immunoprecipitation in hepatocellular carcinoma cells; this interaction is disrupted by benzyl isothiocyanate treatment. CNOT2 overexpression rescues glycolytic enzyme expression (HK2) and apoptosis suppression, placing CNOT2 upstream of c-Myc and STAT3 in this signaling axis. Co-immunoprecipitation, siRNA knockdown, overexpression rescue, Western blot for glycolytic markers and apoptotic markers Scientific reports Low 41629418
2026 CNOT2 physically interacts with VEGF by co-immunoprecipitation in cervical cancer HeLa cells, and ectopic CNOT2 expression upregulates VEGF while CNOT2 depletion suppresses VEGF expression and secretion, establishing a CNOT2–VEGF regulatory axis that promotes angiogenesis and invasion. Co-immunoprecipitation, siRNA knockdown, overexpression, VEGF luciferase reporter assay, cycloheximide chase assay, tube formation assay, CAM assay Scientific reports Low 42045595

Source papers

Stage 0 corpus · 36 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1994 NOT1(CDC39), NOT2(CDC36), NOT3, and NOT4 encode a global-negative regulator of transcription that differentially affects TATA-element utilization. Genes & development 183 7926748
1999 The CCR4 and CAF1 proteins of the CCR4-NOT complex are physically and functionally separated from NOT2, NOT4, and NOT5. Molecular and cellular biology 137 10490603
2011 CNOT2 depletion disrupts and inhibits the CCR4-NOT deadenylase complex and induces apoptotic cell death. Genes to cells : devoted to molecular & cellular mechanisms 70 21299754
2012 Cnot1, Cnot2, and Cnot3 maintain mouse and human ESC identity and inhibit extraembryonic differentiation. Stem cells (Dayton, Ohio) 65 22367759
2017 CNOT2 promotes proliferation and angiogenesis via VEGF signaling in MDA-MB-231 breast cancer cells. Cancer letters 63 29024811
2013 Structure and RNA-binding properties of the Not1-Not2-Not5 module of the yeast Ccr4-Not complex. Nature structural & molecular biology 63 24121231
2004 Repression of promoter activity by CNOT2, a subunit of the transcription regulatory Ccr4-not complex. The Journal of biological chemistry 55 14707134
1984 A relationship between the yeast cell cycle genes CDC4 and CDC36 and the ets sequence of oncogenic virus E26. Nature 52 6374468
1986 Nucleotide sequence of the yeast cell division cycle start genes CDC28, CDC36, CDC37, and CDC39, and a structural analysis of the predicted products. Nucleic acids research 46 3018676
2016 CCR4-Not Complex Subunit Not2 Plays Critical Roles in Vegetative Growth, Conidiation and Virulence in Watermelon Fusarium Wilt Pathogen Fusarium oxysporum f. sp. niveum. Frontiers in microbiology 37 27695445
1990 CDC36 and CDC39 are negative elements in the signal transduction pathway of yeast. Cell regulation 36 2099190
1990 Mutations in cell division cycle genes CDC36 and CDC39 activate the Saccharomyces cerevisiae mating pheromone response pathway. Molecular and cellular biology 35 2111445
1983 Isolation and transcriptional characterization of three genes which function at start, the controlling event of the Saccharomyces cerevisiae cell division cycle: CDC36, CDC37, and CDC39. Molecular and cellular biology 35 6346060
2002 Characterization of mutations in NOT2 indicates that it plays an important role in maintaining the integrity of the CCR4-NOT complex. Journal of molecular biology 34 12215412
2006 Involvement of the SMRT/NCoR-HDAC3 complex in transcriptional repression by the CNOT2 subunit of the human Ccr4-Not complex. The Biochemical journal 33 16712523
2020 Colocalization of MID1IP1 and c-Myc is Critically Involved in Liver Cancer Growth via Regulation of Ribosomal Protein L5 and L11 and CNOT2. Cells 32 32316188
1996 Differential activation of the clustered homeobox genes CNOT2 and CNOT1 during notogenesis in the chick. Developmental biology 31 8954724
2021 Inhibition of CNOT2 Induces Apoptosis via MID1IP1 in Colorectal Cancer Cells by Activating p53. Biomolecules 22 34680125
2019 CNOT2 Is Critically Involved in Atorvastatin Induced Apoptotic and Autophagic Cell Death in Non-Small Cell Lung Cancers. Cancers 20 31574980
2015 CCR4-NOT2 Promotes the Differentiation and Lipogenesis of 3T3-L1 Adipocytes via Upregulation of PPARx03B3;, CEBPα and Inhibition of P-GSK3α/β and β-Catenin. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 18 26584287
2017 CNOT2 promotes degradation of p62/SQSTM1 as a negative regulator in ATG5 dependent autophagy. Oncotarget 14 28537904
2022 Ophiopogonin D increase apoptosis by activating p53 via ribosomal protein L5 and L11 and inhibiting the expression of c-Myc via CNOT2. Frontiers in pharmacology 13 36569330
2019 A heterozygous, intragenic deletion of CNOT2 recapitulates the phenotype of 12q15 deletion syndrome. American journal of medical genetics. Part A 10 31145527
2019 CNOT2 facilitates dengue virus infection via negatively modulating IFN-Independent Non-Canonical JAK/STAT pathway. Biochemical and biophysical research communications 10 31155293
2005 The cyclin-dependent kinase 11 interacts with NOT2. Biochemical and biophysical research communications 10 16039607
2021 Circular RNA CNOT2 knockdown regulates twist family BHLH transcription factor via targeting microRNA 409-3p to prevent breast cancer invasion, migration and epithelial-mesenchymal transition. Bioengineered 8 34698000
2019 CNOT2 as the critical gene for phenotypes of 12q15 microdeletion syndrome. American journal of medical genetics. Part A 7 30768759
2023 Momordicae Semen inhibits migration and induces apoptotic cell death by regulating c-Myc and CNOT2 in human pancreatic cancer cells. Scientific reports 5 37550432
2022 Delineation of the clinical profile of CNOT2 haploinsufficiency and overview of the IDNADFS phenotype. Clinical genetics 5 36224108
2020 MiRNA 3613-5p and MiRNA 3916 rescued the inhibition of cell migration in CNOT2 depleted MDA-MD-231 cells. Translational cancer research 4 35117819
2021 Regulation of CCR4-NOT complex deadenylase activity and cellular responses by MK2-dependent phosphorylation of CNOT2. RNA biology 2 35129087
2025 Study on the mechanism of LNC004268 regulating sheep myoblast proliferation and differentiation through hnRNPK-CNOT2 Axis. International journal of biological macromolecules 1 40774498
2025 Elucidating the Role of CNOT2 in Regulating Cancer Cell Growth via the Modulation of p53 and c-Myc Expression. Current issues in molecular biology 1 40864769
2021 Genome-Wide Study of NOT2_3_5 Protein Subfamily in Cotton and Their Necessity in Resistance to Verticillium wilt. International journal of molecular sciences 1 34073210
2026 CNOT2 /c-Myc/STAT3 signaling is critically involved in glycolysis mediated apoptosis of benzyl isothiocyanate in hepatocellular carcinoma. Scientific reports 0 41629418
2026 Targeting the CNOT2/VEGF pathway by Cornin attenuates angiogenesis and invasion in cervical cancer cells. Scientific reports 0 42045595

Missed literature

Know a paper Affinage missed for CNOT2? Flag it for the maintainers and the community.

No submissions yet.