B lymphocytes differentially use the Rel and nuclear factor kappaB1 (NF-kappaB1) transcription factors to regulate cell cycle progression and apoptosis in quiescent and mitogen-activated cells.
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NF-kappa B inhibition causes spontaneous apoptosis in Epstein-Barr virus-transformed lymphoblastoid cellsMedical immunology: a new journal for a new subspecialty.NF-kB inhibitor blocks B cell development at two checkpointsTo be, or not to be: NF-kappaB is the answer--role of Rel/NF-kappaB in the regulation of apoptosisEnhanced B cell expansion, survival, and humoral responses by targeting death receptor 6A p38 MAPK-MEF2C pathway regulates B-cell proliferationIkappaB kinase signaling is essential for maintenance of mature B cellsInhibition of NF-kappaB activation in vivo impairs establishment of gammaherpesvirus latency.RNAi-mediated c-Rel silencing leads to apoptosis of B cell tumor cells and suppresses antigenic immune response in vivo.Meningococcal porin PorB prevents cellular apoptosis in a toll-like receptor 2- and NF-kappaB-independent mannerGenetic approaches in mice to understand Rel/NF-kappaB and IkappaB function: transgenics and knockouts.Roles of the NF-kappaB pathway in lymphocyte development and function.NF-kappaB controls cell growth and differentiation through transcriptional regulation of cyclin D1.The role of nuclear factor-kappaB essential modulator (NEMO) in B cell development and survival.Interferon induces NF-kappa B-inducing kinase/tumor necrosis factor receptor-associated factor-dependent NF-kappa B activation to promote cell survival.The combined absence of NF-kappa B1 and c-Rel reveals that overlapping roles for these transcription factors in the B cell lineage are restricted to the activation and function of mature cells.IKK-induced NF-κB1 p105 proteolysis is critical for B cell antibody responses to T cell-dependent antigen.NF-kappaB1 can inhibit v-Abl-induced lymphoid transformation by functioning as a negative regulator of cyclin D1 expression.Unique CD40-mediated biological program in B cell activation requires both type 1 and type 2 NF-kappaB activation pathways.Novel targeted deregulation of c-Myc cooperates with Bcl-X(L) to cause plasma cell neoplasms in mice.The anti-apoptotic activities of Rel and RelA required during B-cell maturation involve the regulation of Bcl-2 expression.NF-kappaB family of transcription factors: central regulators of innate and adaptive immune functions.A multi-scale approach reveals that NF-κB cRel enforces a B-cell decision to divide.Rel-dependent induction of A1 transcription is required to protect B cells from antigen receptor ligation-induced apoptosisNfkb1 activation by the E26 transformation-specific transcription factors PU.1 and Spi-B promotes Toll-like receptor-mediated splenic B cell proliferation.NF-κB in immunobiology.The c-Rel Transcription Factor in Development and Disease.Rewiring of sIgM-mediated intracellular signaling through the CD180 Toll-like receptor.The combined absence of the transcription factors Rel and RelA leads to multiple hemopoietic cell defects.DNA-damage response network at the crossroads of cell-cycle checkpoints, cellular senescence and apoptosisFunctions of NF-kappaB1 and NF-kappaB2 in immune cell biologyNF-kappaB1 and c-Rel cooperate to promote the survival of TLR4-activated B cells by neutralizing Bim via distinct mechanisms.B cell-associated immune profiles in patients with end-stage renal disease (ESRD)Rel induces interferon regulatory factor 4 (IRF-4) expression in lymphocytes: modulation of interferon-regulated gene expression by rel/nuclear factor kappaB.Bruton's tyrosine kinase is required for activation of IkappaB kinase and nuclear factor kappaB in response to B cell receptor engagement.Attenuation of apoptosis underlies B lymphocyte stimulator enhancement of humoral immune response.Constitutive nuclear factor kappaB activity is required for survival of activated B cell-like diffuse large B cell lymphoma cellsMouse plasmacytoid cells: long-lived cells, heterogeneous in surface phenotype and function, that differentiate into CD8(+) dendritic cells only after microbial stimulusNuclear factor kappa B is required for the development of marginal zone B lymphocytes.Inhibition of astroglial nuclear factor kappaB reduces inflammation and improves functional recovery after spinal cord injury.
P2860
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P2860
B lymphocytes differentially use the Rel and nuclear factor kappaB1 (NF-kappaB1) transcription factors to regulate cell cycle progression and apoptosis in quiescent and mitogen-activated cells.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年学术文章
@wuu
1998年学术文章
@zh-cn
1998年学术文章
@zh-hans
1998年学术文章
@zh-my
1998年学术文章
@zh-sg
1998年學術文章
@yue
1998年學術文章
@zh
1998年學術文章
@zh-hant
name
B lymphocytes differentially u ...... t and mitogen-activated cells.
@ast
B lymphocytes differentially u ...... t and mitogen-activated cells.
@en
type
label
B lymphocytes differentially u ...... t and mitogen-activated cells.
@ast
B lymphocytes differentially u ...... t and mitogen-activated cells.
@en
prefLabel
B lymphocytes differentially u ...... t and mitogen-activated cells.
@ast
B lymphocytes differentially u ...... t and mitogen-activated cells.
@en
P2093
P2860
P356
P1476
B lymphocytes differentially u ...... t and mitogen-activated cells.
@en
P2093
P2860
P304
P356
10.1084/JEM.187.5.663
P407
P577
1998-03-01T00:00:00Z