Pages that link to "Q35199327"
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The following pages link to Oncovirus Kaposi sarcoma herpesvirus (KSHV) represses tumor suppressor PDLIM2 to persistently activate nuclear factor κB (NF-κB) and STAT3 transcription factors for tumorigenesis and tumor maintenance (Q35199327):
Displaying 15 items.
- A Central Role for STAT3 in Gammaherpesvirus-Life Cycle and -Diseases (Q26741576) (← links)
- KSHV-Mediated Angiogenesis in Tumor Progression (Q26742030) (← links)
- Viral Interactions with PDZ Domain-Containing Proteins-An Oncogenic Trait? (Q26770053) (← links)
- Global Proteome and Phospho-proteome Analysis of Merlin-deficient Meningioma and Schwannoma Identifies PDLIM2 as a Novel Therapeutic Target. (Q33809716) (← links)
- NF-κB1 p105 suppresses lung tumorigenesis through the Tpl2 kinase but independently of its NF-κB function (Q35994472) (← links)
- Kaposi's sarcoma herpesvirus (KSHV) microRNA K12-1 functions as an oncogene by activating NF-κB/IL-6/STAT3 signaling (Q37362933) (← links)
- Inactivation of the putative ubiquitin-E3 ligase PDLIM2 in classical Hodgkin and anaplastic large cell lymphoma (Q37683382) (← links)
- DNA Tumor Virus Regulation of Host DNA Methylation and Its Implications for Immune Evasion and Oncogenesis (Q50042001) (← links)
- Myeloid STAT3 Promotes Lung Tumorigenesis by Transforming Tumor Immunosurveillance into Tumor-Promoting Inflammation. (Q51176869) (← links)
- Modulation of Cellular CpG DNA Methylation by Kaposi's Sarcoma-Associated Herpesvirus (Q59358871) (← links)
- STAT3 Interactors as Potential Therapeutic Targets for Cancer Treatment (Q59618020) (← links)
- HCV and flaviviruses hijack cellular mechanisms for nuclear STAT2 degradation: Up-regulation of PDLIM2 suppresses the innate immune response (Q66678745) (← links)
- Causative role of PDLIM2 epigenetic repression in lung cancer and therapeutic resistance (Q91404355) (← links)
- PDZ Domains as Drug Targets (Q92102996) (← links)
- KSHV-encoded LANA protects the cellular replication machinery from hypoxia induced degradation (Q93074235) (← links)