| 1994 |
Yeast Nop2p (ortholog of human NOP2/p120) is an essential nucleolar protein required for cell viability; it localizes primarily to the nucleolus as determined by indirect immunofluorescence and nuclear fractionation, and its overexpression alters nucleolar morphology (detachment from nuclear envelope, fragmentation) without affecting ribosome subunit synthesis levels. |
Indirect immunofluorescence, subcellular fractionation, electron microscopy, GAL10-driven overexpression, SDS-PAGE |
The Journal of cell biology |
High |
7806561
|
| 2001 |
Temperature-sensitive nop2 alleles in S. cerevisiae cause defective processing of 27S pre-rRNA to mature 25S rRNA and dramatic reductions in 60S ribosome subunits under non-permissive conditions, without significantly affecting 40S subunits or 18S rRNA, establishing Nop2p as a trans-acting factor required for large ribosomal subunit biogenesis and rRNA processing. |
Molecular genetics (temperature-sensitive alleles), ribosome subunit analysis, pre-rRNA processing assays |
Nucleic acids research |
High |
11452018
|
| 2014 |
LncRNA-hPVT1 binds to NOP2 protein (identified by RNA pulldown and mass spectrometry) and enhances stability of NOP2 protein, with NOP2 being required for PVT1-mediated promotion of HCC cell proliferation, cell cycling, and stem cell-like properties. |
RNA pulldown, mass spectrometry, gain-of-function and loss-of-function experiments |
Hepatology (Baltimore, Md.) |
Medium |
25043274
|
| 2015 |
RNAi-mediated knockdown of Nop2 in mouse preimplantation embryos causes developmental arrest at morula stage with reduced blastomere numbers, increased apoptosis, impaired cell-lineage specification, and global reduction of all RNA species including rRNA, snRNA, snoRNA, and mRNA, demonstrating that NOP2 is required for RNA processing and/or stability during preimplantation development. |
RNAi knockdown in mouse embryos, RNA quantification, apoptosis assays, lineage marker analysis |
Molecular reproduction and development |
Medium |
26632338
|
| 2016 |
NOL1 (NOP2) was identified as a TERC-binding protein associated with catalytically active telomerase; NOL1 binds to the TCF-binding element of the cyclin D1 promoter and activates its transcription; telomerase is recruited to the cyclin D1 promoter in a TERC-dependent manner through interaction with NOL1, further enhancing cyclin D1 transcription; depletion of NOL1 suppresses cyclin D1 promoter activity and induces growth arrest and altered cell cycle distributions. |
Co-immunoprecipitation, chromatin immunoprecipitation (ChIP), promoter reporter assays, siRNA knockdown |
Journal of cell science |
Medium |
26906424
|
| 2019 |
NOP2 depletion in mouse preimplantation embryos disrupts nucleolar maturation (increased nucleolus precursor body ratio, decreased nucleolus size ratio by TEM) and reduces rRNA abundance (by qPCR and FISH), impairs first lineage specification (reduced TEAD4, NANOG, KLF4), with conserved function confirmed in bovine embryos. |
RNAi knockdown, transmission electron microscopy, RNA-seq, FISH, qPCR, immunofluorescence |
FASEB journal |
Medium |
31908012
|
| 2020 |
NOP2 suppresses HIV-1 transcription and promotes viral latency by: (1) associating with HIV-1 5' LTR chromatin, (2) competing with HIV-1 Tat protein for binding to TAR RNA, and (3) contributing to m5C methylation of TAR RNA; the RNA methyltransferase catalytic domain (MTD) of NOP2 mediates its competition with Tat and binding with TAR. |
Loss- and gain-of-function analyses, chromatin immunoprecipitation, RNA immunoprecipitation, RNA methylation assays, domain mutagenesis, HIV-1 latency reactivation assays |
PLoS pathogens |
High |
32176734
|
| 2022 |
Human NOP2/NSUN1 catalyzes deposition of m5C at position 4447 on 28S rRNA (identified by miCLIP-seq); NOP2/NSUN1 also binds the 5'ETS region of pre-rRNA and regulates pre-rRNA processing through non-catalytic complex formation with box C/D snoRNAs (U3 and U8), facilitating their recruitment to pre-90S ribosomal particles and stable assembly into snoRNP complexes; both WT and catalytically inactive NOP2/NSUN1 rescue rRNA processing defects and snoRNP assembly in knockdown background, demonstrating m5C catalytic activity is dispensable for ribosome biogenesis. |
miCLIP-seq, siRNA knockdown, complementation with WT and catalytic mutant, snoRNP assembly assays, pre-rRNA processing analysis |
Nucleic acids research |
High |
36161484
|
| 2023 |
NOP2 catalyzes m5C modification of c-Myc mRNA in an EIF3A-dependent manner; m5C methylation of c-Myc mRNA induces its degradation dependent on EIF3A, thereby reducing c-Myc expression and reprogramming glucose metabolism; MAZ transcription factor directly controls NOP2 expression in HCC. |
m5C methylation assays, RNA immunoprecipitation, RNA stability assays, EIF3A co-functional experiments, ChIP for MAZ binding, loss-of-function assays |
Research (Washington, D.C.) |
Medium |
37398932
|
| 2023 |
NOP2 methylates XPD mRNA at m5C sites, enhancing XPD mRNA stability; NOP2 overexpression elevated XPD expression and inhibited HCC cell proliferation, migration, and invasion in vitro. |
m5C methylation assays, RNA stability assays, in vitro functional assays |
Neoplasma |
Low |
37498063
|
| 2023 |
NAT10-mediated ac4C modification of Nop2 mRNA stabilizes it and enhances translation; NAT10 knockdown decreases ac4C on Nop2 mRNA and reduces NOP2 RNA and protein abundance; NOP2 depletion inhibits translation of transcription factor TEAD4, leading to defective Cdx2 expression and failure of trophectoderm fate specification; exogenous Nop2 mRNA partially rescues abnormal development. |
acRIP-PCR, single-cell sequencing, RNA-seq, embryonic phenotype monitoring, mRNA rescue experiments |
Cellular and molecular life sciences |
Medium |
37768430
|
| 2024 |
NOP2 deposits m5C on EZH2 mRNA, stabilizing it in an ALYREF (m5C reader)-dependent manner; NOP2/ALYREF/EZH2 axis promotes EMT in lung cancer cells; EZH2 counteracts NOP2 effects on H3K27me3 occupancy at the E-cadherin promoter, repressing E-cadherin expression. |
RNA-seq, methylated RNA immunoprecipitation (MeRIP), RNA stability assays, ChIP, in vitro and in vivo functional assays |
Cell death & disease |
Medium |
39013911
|
| 2024 |
NOP2 stimulates m5C modification of APOL1 mRNA; m5C reader YBX1 recognizes and binds the m5C site in the 3'-UTR of APOL1 mRNA, stabilizing it; NOP2/APOL1 axis activates PI3K-Akt signaling to promote ccRCC progression. |
m5C bisulfite sequencing, RNA-seq, RIP/MeRIP RT-qPCR, luciferase reporter assay, RNA stability assay, loss/gain-of-function assays |
International journal of biological sciences |
Medium |
39309431
|
| 2025 |
NSUN1 (NOP2) isoform 3 selectively interacts with TDP-43 independently of RNA in human cells; aberrant Nsun1 activity drives TDP-43-induced m5C-RNA hypermethylation in a Drosophila model; Nsun1 downregulation alleviates TDP-43-induced neurodegeneration, lifespan deficits, and cytoplasmic accumulation of TDP-43; NSUN1 is nucleolar and interacts with TDP-43 in both nucleolar and nucleoplasmic compartments. |
TDP-43 interactome mapping (co-IP/MS), Drosophila genetic epistasis, m5C-RNA quantification, isoform-specific interaction assays, postmortem human brain analysis |
Life science alliance |
Medium |
41188020
|
| 2025 |
NOP2 catalyzes m5C modification of COL1A1 mRNA, stabilizing it; tranilast treatment reduces NOP2 expression and directly interacts with NOP2 (by RIP), decreasing m5C on COL1A1 mRNA, reducing COL1A1 expression, and suppressing hypertrophic scar fibroblast proliferation, migration, and invasion. |
MeRIP, RIP, dual luciferase reporter assay, dot blot, cell functional assays |
Tissue & cell |
Low |
41260007
|
| 2026 |
NOP2 knockout in zebrafish (CRISPR/Cas9) causes embryonic lethality within 3-5 dpf with microcephaly and cerebral edema; nop2 deficiency impairs differentiation of neural progenitors, activates p53-dependent apoptosis in neural cells, and compromises pre-ribosomal particle processing; genetic epistasis shows tp53 mutation partially rescues neurogenic defects and cerebral edema but not microcephaly, establishing ribosome biogenesis defects as the primary molecular lesion upstream of p53 apoptosis. |
CRISPR/Cas9 knockout, Ribo-seq, ribosome processing assays, p53 epistasis experiments, histology/immunostaining |
FASEB journal |
Medium |
41631357
|
| 2026 |
NOP2 promotes glycolysis in larynx cancer by depositing m5C on TPI1 mRNA, stabilizing it; NOP2 silencing reduces m5C modification on TPI1 mRNA and decreases TPI1 mRNA stability; overexpression of TPI1 rescues impaired glycolysis caused by NOP2 knockdown. |
MeRIP, RIP, dual-luciferase reporter assay, RNA stability assay, functional metabolic assays, xenograft models |
Molecular carcinogenesis |
Low |
41498196
|
| 2026 |
NOP2 deposits m5C on LMNB2 mRNA, enhancing its stability and elevating LMNB2 protein levels; LMNB2 overexpression rescues the suppressed malignant phenotypes induced by NOP2 knockdown in colorectal cancer cells, establishing LMNB2 as a critical downstream effector of NOP2. |
MeRIP-seq, RIP-seq, transcriptomic sequencing, RNA stability assays, rescue overexpression experiments, in vitro and in vivo functional assays |
Cancer medicine |
Low |
40366008
|
| 2026 |
NOP2-mediated m5C deposition on SCD mRNA facilitates recruitment of m5C reader YBX1, stabilizing SCD mRNA and boosting SCD expression; the NOP2/YBX1/SCD axis orchestrates lipid metabolism reprogramming (altering saturated, monounsaturated, and polyunsaturated fatty acid distribution) to suppress lipid peroxidation and protect bladder cancer cells from ferroptosis. |
MeRIP, RIP, RNA stability assays, lipid profiling, in vitro and xenograft functional assays |
International journal of biological sciences |
Low |
42088435
|
| 2026 |
NOP2 stabilizes NFKB1 mRNA through m5C modification; NOP2 knockdown inhibits NFKB1 transcription by decreasing m5C modification on NFKB1 mRNA; NFKB1 overexpression restores inflammation and apoptosis inhibited by NOP2 knockdown in LPS-induced bronchial epithelial cells, establishing a NOP2/m5C/NFKB1 axis in COPD. |
MeRIP, RNA stability assays, rescue overexpression, in vivo rat COPD model, cytokine measurement |
Journal of biochemical and molecular toxicology |
Low |
41766206
|
| 2026 |
In MYC-driven liver cancer cells, NOP2 (rRNA m5C-methyltransferase) expression is regulated by both MYC overexpression and methionine abundance; NOP2 knockdown reduces methylation of multiple 28S rRNA residues and selectively inhibits MYC-driven (but not RAS-driven) liver cancer cell proliferation and in vivo tumor growth. |
Heavy isotope methionine tracing, NOP2 knockdown, rRNA methylation analysis, in vivo tumor growth assays, methionine depletion experiments |
bioRxivpreprint |
Medium |
41659612
|