CDKN2C antibody Polyclonal Antibodies Primary antibodies
- Known as:
- CDKN2C (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100080
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- CDKN2C antibody Polyclonal Antibodies Primary antibodies
Related genes to: CDKN2C antibody Polyclonal Antibodies Primary antibodies
- 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 Polyclonal Antibodies Primary antibodies
Related articles to: CDKN2C antibody Polyclonal Antibodies Primary antibodies
- EBV employs multiple strategies to subvert host innate immunity, including suppression of type I IFN signaling. However, the precise mechanism by which its latent oncoprotein LMP1 modulates this pathway in nasopharyngeal carcinoma (NPC) remains unclear. Here, we demonstrated that LMP1 enhances the interaction between interferon regulatory factor 3 (IRF3) and E3 ubiquitin ligase Ro52, which leads to the degradation of IRF3 protein. Low IRF3 expression correlates with poor prognosis in NPC patients. Notably, IRF3 may inhibit cell G1/S transition by directly inducing CDKN2C transcription, which suggests the direct effect as a moonlighting protein in regulating cell cycle. Cisplatin is an effective DNA-damaging anti-tumor agent which may activate type I IFNs-mediated anti-tumor immunity by stimulating the release of dsDNA. EBV (LMP1) inhibits cisplatin-activated type I IFN signaling by reducing IRF3 expression. The activation of IRF3 enhances the sensitivity of EBV (LMP1)-positive NPC cells to cisplatin in vitro and in vivo. These findings establish the LMP1-Ro52-IRF3 axis as a critical immune evasion mechanism that drives cisplatin resistance and suggest that targeting this axis represents a viable strategy to enhance chemotherapy efficacy in EBV-positive NPC. - Source: PubMed
Publication date: 2026/05/15
Li YueshuoLiu NaYang ChenxingHe ShanLuo ChengWang LinTang MinLuo XiangjianCao YaShang LiShi Feng - Hyperthermic intraperitoneal chemotherapy (HIPEC) for colorectal peritoneal metastases relies primarily on DNA-damaging agents whose efficacy depends on sustained cytotoxic exposure. Whether brief treatment can induce durable transcriptional remodeling remains unclear. Mithramycin A (MA) is a GC-rich DNA-binding agent with transcriptional regulatory activity involving chromatin-associated pathways. Here, we investigated the molecular and functional consequences of a single 90-min HIPEC-mimetic MA exposure in colorectal cancer models. RNA sequencing revealed extensive and coordinated transcriptional remodeling, affecting a substantial fraction of expressed genes and producing a response qualitatively distinct from mitomycin C. MA selectively suppressed key chromatin-associated regulatory factors, including DNMT1, JARID2, and HDAC4, while coordinately activating canonical cyclin-dependent kinase inhibitors CDKN1A, CDKN1C, and CDKN2C. Gene set enrichment analysis demonstrated enrichment of G2/M checkpoint pathways and suppression of oncogenic gene networks. These molecular changes translated into sustained inhibition of clonogenic growth and activation of caspase-dependent apoptosis following drug washout, with hyperthermia potentiating apoptotic signaling. Collectively, these findings indicate that brief MA exposure induces selective modulation of chromatin regulators and durable transcriptional reorganization, supporting modulation of chromatin regulatory networks as a potential therapeutic strategy for HIPEC-based colorectal cancer therapy. - Source: PubMed
Publication date: 2026/04/17
Coburn-Flynn OliviaButchy M VirginiaGhanem YazidEmery RobertVerchio VincentKnapp KristenCollier JessicaJethi SahilSpitz Francis RZhang PingElbezanti Weam OthmanHong Young Ki - Head and neck squamous cell carcinoma (HNSC) remains one of the main causes of cancer-related deaths among male patients with cancer. Although surgery, chemotherapy, radiotherapy, targeted therapy, and immunotherapy are available, their success in controlling the disease remains limited. Novel targets and therapeutics for HNSC therefore await identification, which is frequently pursued using bioinformatics approaches. - Source: PubMed
Hung Yu-HsuanWang Min-HongChen Li-TzongPan Mei-RenWang Hui-ChingMoi Sin-HuaLuo Chi-Wen - 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