Ask about this productRelated genes to: CDKN2C antibody
- Gene:
- CDKN2C NIH gene
- Name:
- cyclin dependent kinase inhibitor 2C
- Previous symbol:
- -
- Synonyms:
- INK4C, p18
- Chromosome:
- 1p32.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-07-06
- Date modifiied:
- 2016-06-08
Related products to: CDKN2C antibody
Related articles to: CDKN2C antibody
- Epstein-Barr virus (EBV) persistently infects over 95% of adults worldwide and is associated with a range of cancers, including lymphomas and epithelial malignancies. Despite advances in understanding EBV biology, targeted therapies for EBV-associated cancers remain limited. To identify novel dependencies in EBV-infected cancers, we performed genome-wide CRISPR-Cas9 loss-of-function screens in EBV+ lymphoblastoid versus Burkitt lymphoma cells, which differ by EBV latency programs. JunB emerged as a critical LCL-selective host dependency factor. LCL JunB knockout significantly decreased proliferation, with reduced G2/M progression, but without inducing apoptosis. JunB was more highly expressed in B cells with the EBV latency III than latency I program and correlated with LMPist1 levels in newly infected B cells. LMP1 stimulated JunB expression in a manner dependent on its cytoplasmic tail TES1/CTAR1 region and on canonical NF-κB. EBV-activated JunB played an obligatory role in repression of the G1/S phase inhibitor /p18 in LCLs but not Burkitt B cells. These findings establish an LMP1-JunB-p18 axis as essential for EBV-driven lymphoblastoid B cell proliferation, suggest JunB-mediated cross-talk between Epstein-Barr nuclear antigens and LMP1, and highlight JunB as a potential therapeutic target for EBV-associated lymphoproliferative disorders. - Source: PubMed
Publication date: 2026/04/01
Burton Eric MLiao YifeiMaestri DavideMitra BidishaGewurz Benjamin E - Leukemic conversion of nodal mantle cell lymphoma (MCL) is most often detected as incidental lymphocytosis on routine blood counts, often mimicking chronic lymphocytic leukemia, with flow cytometric immunophenotyping being the gold-standard test for diagnosis. Blastoid MCL closely mimics acute lymphoblastic leukemia (ALL), thus posing significant diagnostic challenges. Blastoid transformation of MCL is usually associated with mutations, homozygous deletions of and , amplifications and overexpression of ,and occasionally microdeletions of , and is associated with an aggressive disease course. Equivocal cases require histopathological evaluation, fluorescent in-situ hybridization, or molecular studies for confirmation. We report the case of an 82-year-old female who presented with lower respiratory tract infection and was found to have severe anemia (hemoglobin: 45 g/L) and marked leukocytosis (325 × 10⁹/L) with 63% blastoid-appearing cells on peripheral blood smear, initially suggestive of acute leukemia. Flow cytometric immunophenotyping demonstrated bright CD45 expression with low side scatter and positivity for CD19, CD20, CD38, CD5, CD79b, and FMC7 with negativity for CD34, CD23, CD200, and CD10, suggesting blastoid transformation of MCL rather than de novo ALL. This case highlights the critical role of flow cytometry in distinguishing blastoid MCL from acute leukemia, thereby preventing misdiagnosis and ensuring appropriate therapeutic decision-making. - Source: PubMed
Publication date: 2026/02/16
Kundu AnirbanGiri SulagnaBasu Atoshi - Sjögren's disease (SjD) is a group of chronic autoimmune diseases primarily targeting exocrine glands, including the lacrimal glands (LG). Involvement of the lacrimal glands leads to severe dry eye, also known as Sjögren's disease-associated dry eye (SjD-DE). Current, available animal models of SjD are achieved by using autoantigens from salivary gland. This study establishes a novel lacrimal gland-specific autoimmune model that recapitulates key features of SjD-DE, providing a tool for investigating LG-focused mechanisms in SjD. - Source: PubMed
Publication date: 2026/02/13
Li SiyuanLiu ShanLi YaqiongZhang PengLei FengyangTian LeiJie Ying - Enhancer RNAs (eRNAs) are best known for their role in transcriptional regulation, where they facilitate enhancer-promoter communication and chromatin remodeling. Yet growing evidence suggests that their function may extend beyond the nucleus. Here, we systematically characterize the decay kinetics of eRNAs across human cell types using time-resolved transcriptomics and kinetic modeling. While most eRNAs undergo canonical exponential decay, a subset displays nonlinear dynamics, suggesting context-dependent degradation mechanisms. Perturbation of core decay regulators, including components of the mA and pathways, reveals that eRNA stability is modulated by a patchwork of pathways governing mRNA turnover. Integrating transcriptome-wide ribosome profiling, RNA-seq, and half-life data, we identify eRNAs associated with changes in mRNA stability and translation efficiency of their target protein-coding transcripts. Functional validation of one such eRNA, , shows that it regulates and mRNA independently of transcription and impacts cell migration. These findings redefine the regulatory scope of eRNAs, positioning them as active participants in post-transcriptional gene control and cellular behavior. The resulting decay profiles and regulatory annotations have been incorporated into the eRNAkit database, available at https://github.com/AneneLab/eRNAkit, enhancing its capacity for integrative systems-level analysis of eRNA function. - Source: PubMed
Publication date: 2026/04/16
Kuklinkova ReneBenova NataliaAnene Chinedu A - Chromosomal aberrations in tumors are key indicators of genomic instability and important drivers of neoplasia. While chromosomal changes in uterine leiomyomas have been studied for decades, comprehensive evaluation of chromosomal aberrations in uterine leiomyomas on the scale of modern tumor research has been lacking. - Source: PubMed
Publication date: 2026/01/16
Ilves SiniJokinen ViljaKatainen RikuSiili EmmaBützow RalfHeikinheimo OskariPasanen AnnukkaKarhu AuliVälimäki NikoAaltonen Lauri A