Deletion of either C-terminal transactivation subdomain enhances the in vitro transforming activity of human transcription factor REL in chicken spleen cells.
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The c-Rel transcription factor and B-cell proliferation: a deal with the devilc-Rel deficiency increases caspase-4 expression and leads to ER stress and necrosis in EBV-transformed cellsRNAi-mediated c-Rel silencing leads to apoptosis of B cell tumor cells and suppresses antigenic immune response in vivo.Overexpression of an activated REL mutant enhances the transformed state of the human B-lymphoma BJAB cell line and alters its gene expression profileSer484 and Ser494 in REL are the major sites of IKK phosphorylation in vitro: evidence that IKK does not directly enhance GAL4-REL transactivation.Deletion analysis and alternative splicing define a transactivation inhibitory domain in human oncoprotein RELHistone acetyltransferase p300 is a coactivator for transcription factor REL and is C-terminally truncated in the human diffuse large B-cell lymphoma cell line RC-K8.Characterization of the core elements of the NF-κB signaling pathway of the sea anemone Nematostella vectensis.The c-Rel Transcription Factor in Development and Disease.The NF-κB subunit c-Rel regulates Bach2 tumour suppressor expression in B-cell lymphomaCAPERalpha is a novel Rel-TAD-interacting factor that inhibits lymphocyte transformation by the potent Rel/NF-kappaB oncoprotein v-Rel.Alternative splicing in the NF-kappaB signaling pathway.Peptidyl-prolyl isomerase Pin1 markedly enhances the oncogenic activity of the rel proteins in the nuclear factor-kappaB family.A rearranged EP300 gene in the human B-cell lymphoma cell line RC-K8 encodes a disabled transcriptional co-activator that contributes to cell growth and oncogenicity.Evidence for an oncogenic modifier role for mutant histone acetyltransferases in diffuse large B-cell lymphoma.The p53 homologue DeltaNp63alpha interacts with the nuclear factor-kappaB pathway to modulate epithelial cell growth.Mutation of an IKK phosphorylation site within the transactivation domain of REL in two patients with B-cell lymphoma enhances REL's in vitro transforming activity.Human Pax-5 C-terminal isoforms possess distinct transactivation properties and are differentially modulated in normal and malignant B cells.An optimal range of transcription potency is necessary for efficient cell transformation by c-Rel to ensure optimal nuclear localization and gene-specific activation.The Direct and Indirect Roles of NF-κB in Cancer: Lessons from Oncogenic Fusion Proteins and Knock-in Mice.
P2860
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P2860
Deletion of either C-terminal transactivation subdomain enhances the in vitro transforming activity of human transcription factor REL in chicken spleen cells.
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2003 nî lūn-bûn
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name
Deletion of either C-terminal ...... r REL in chicken spleen cells.
@en
Deletion of either C-terminal ...... r REL in chicken spleen cells.
@nl
type
label
Deletion of either C-terminal ...... r REL in chicken spleen cells.
@en
Deletion of either C-terminal ...... r REL in chicken spleen cells.
@nl
prefLabel
Deletion of either C-terminal ...... r REL in chicken spleen cells.
@en
Deletion of either C-terminal ...... r REL in chicken spleen cells.
@nl
P2093
P2860
P356
P1433
P1476
Deletion of either C-terminal ...... r REL in chicken spleen cells.
@en
P2093
Daniel T Starczynowski
Joseph G Reynolds
Thomas D Gilmore
P2860
P2888
P304
P356
10.1038/SJ.ONC.1206801
P407
P577
2003-10-01T00:00:00Z