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1 as PR domain-containing 1, with ZNF domain (PRDM1)).
2 other molecules, and the absence of Blimp-1 (prdm1).
3 gnaling through the protein PR/SET domain 1 (PRDM1).
4 e transcription factor Blimp1 (also known as Prdm1).
5 izing the anti-proliferative factor Blimp-1 (Prdm1).
6 igh PRDM1alpha mRNA levels but low levels of PRDM1.
7 igh PRDM1alpha mRNA expression and unmutated PRDM1.
8 phocyte-induced maturation protein (Blimp-1)/PRDM1.
9 yhc3, and all differentiate independently of Prdm1.
10 ession of the transcription factors KLF4 and PRDM1.
11 nner in differentiating B cells and targeted Prdm1.
12 importance of Bcl-6-dependent repression of prdm1.
13 cis-regulatory elements, including those of Prdm1.
14 ntrolled, including GRHL3, ZNF750, KLF4, and PRDM1.
15 urthermore, we show that Blimp1 (also called Prdm1), a let-7 target and a master regulator of PGC spe
18 r responses triggered by VLVs and found that PRDM1, a master regulator in cell differentiation, was s
22 itch fibre characteristics in the absence of Prdm1 activity, whereas those that do not express smyhc1
26 by the activity of the transcription factor Prdm1 (also called Ubo or Blimp1) in response to Hedgeho
27 monstrate that the transcriptional repressor PRDM1 (also known as Blimp-1 or PRDI-BF1) is a critical
28 induction of PR domain-containing protein 1 (PRDM1; also known as Blimp-1), a critical regulator of p
29 In TFH cells, Fgl2 induces the expression of Prdm1 and a panel of checkpoint molecules, including PD1
32 e more accessible in stem-like cells whereas Prdm1 and Id2 were more accessible in exhausted CD8 T ce
34 ates that the functional interaction between PRDM1 and IFN-regulated pathways antedates the evolution
40 on-associated molecules such as Tim-3, Lag3, Prdm1 and Pbx3, and Bat3 knockdown in myelin-antigen-spe
42 hat NANOG can bind and activate enhancers of Prdm1 and Prdm14 in EpiLCs in vitro; BLIMP1 (encoded by
44 and CD38(-) EB cells significantly expressed PRDM1 and TFAP2C, although PRDM1 mRNA in CD38(-) cells l
46 cell fates are regulated in mice, we deleted Prdm1 and Vsx2 or their cell type-specific enhancers sim
48 directly activates the transcription factors Prdm1 and Vsx2 through cell type-specific enhancers.
50 NR4A family of nuclear receptors, as well as Prdm1 and Xbp1 While deletion of Ldha prevented developm
52 he transcription factors Blimp-1 (encoded by Prdm1) and c-Maf co-dominantly regulate Il10 while negat
53 noted as the PRDI-BF1 (HGMW-approved symbol PRDM1) and RIZ (HGMW-approved symbol PRDM2) homologous r
56 hese genes provide evidence that nfat5, fos, prdm1, and dusp16 are novel direct targets of Blimp-1.
58 Inducible, Cre-mediated deletion of Hspa5, Prdm1, and Xbp1 consistently induces cellular stress and
60 ive regulation of NK activation and position PRDM1 as a common regulator of the adaptive and innate i
61 nd the MHC, and identifies a unique role for PRDM1 as a key regulator of Ag presentation by MHC class
63 enetic defect in DLBCL cells and establishes PRDM1 as a potential tumor suppressor gene in DLBCL.
64 transcription factor binding motifs SRF and PRDM1 as important regulators of PIP3-sensitive mRNAs in
65 ified the transcriptional repressor Blimp-1 (PRDM1) as a downstream effector of the NF-kappaB, RelB/B
66 identified the transcription factor Blimp-1 (Prdm1) as a key IL-23-induced factor that drove the infl
67 n through the BCR rapidly induces endogenous PRDM1 at the level of transcription with minor changes i
70 ropean ancestry: CD247, NAB1, PTTG1-MIR146A, PRDM1-ATG5, TNFAIP3, XKR6, MAPT-CRHR1, RPTOR-CHMP6-BAIAP
71 domain containing 1 with zinc finger domain (PRDM1)/B lymphocyte-induced maturation protein 1 (BLIMP1
74 etic lineage development (e.g., HUWE1, IRF4, PRDM1, BATF3, TOX, ID2, IKZF3, and CDK6) or were hematop
75 oma cell lines express the highest levels of PRDM1 beta mRNA relative to the full-length form, while
78 ncreased H3K27 acetylation in cHL, disrupted PRDM1 binding, and co-occurred with BCL6 expression in c
79 in LCLs inhibition of CDKN2C (p18INK4c) and PRDM1 (BLIMP-1) transcription results from direct bindin
83 Over-expression of miR-9 or let-7a reduced PRDM1/Blimp-1 levels in U266 cells by 30% to 50%, wherea
85 nding sites in the 3' untranslated region of PRDM1/blimp-1 mRNA and repressed luciferase reporter act
91 ube and colleagues have identified FOXO3 and PRDM1 (Blimp1) as tumor suppressor genes with a potentia
92 nd Igh enhancers and a distal element at the Prdm1 (Blimp1) locus, E-proteins contributed to Igk, Igh
93 llenge wild-type, Bcl6(fl/fl) Foxp3-Cre, and Prdm1 (Blimp1)(fl/fl) Foxp3-Cre mice to study the recipr
94 AIOLOS), TBX21 (T-bet), NFIL3 (E4BP4), ZEB2, PRDM1 (BLIMP1), and RORA mRNA levels are higher in CD56(
96 ng the zinc finger transcriptional repressor Prdm1/Blimp1 (PR domain containing 1, with ZNF domain; p
97 ls of the plasmablast differentiation marker PRDM1/Blimp1 and increased the abundance of c-Myc protei
98 at the zinc finger transcriptional repressor Prdm1/Blimp1 is essential for specification of spiral ar
100 misexpression and dominant-negative studies, Prdm1/Blimp1 was proposed to promote anterior endomesode
101 by the zinc finger transcriptional repressor Prdm1/Blimp1, an essential regulator of placenta develop
102 5b down-regulates the expression of IRF4 and PRDM1/BLIMP1, and memory B cell-enriched hsa-miR-223 dow
105 Thus, abnormal epigenetic down-regulation of PRDM1 by let-7 and other microRNAs may represent an alte
106 n experiments support a role of targeting of PRDM1 by microRNA let-7 family in mediating this down-re
108 ate and propionate decrease B cell Aicda and Prdm1 by upregulating select miRNAs that target Aicda an
109 n of the master transcription factor Blimp-1/Prdm1 can be observed; when the canonical B cell promote
110 dritic cell-specific conditional knockout of Prdm1 (CKO mice) altered the presentation of antigen to
112 inc-finger transcriptional repressor Blimp1 (Prdm1) controls gene expression patterns during differen
114 ine-specific deletion of Utf1 resulting from Prdm1-Cre mediated recombination are born with significa
115 neage tracing experiments exploiting a novel Prdm1.Cre-LacZ allele demonstrate that these Blimp1(+) c
118 Prdm1 down-regulated IL-2 signaling, whereas Prdm1-deficiency enhanced IL-2 signaling in mouse CD4(+)
121 29 other regions, including TNFAIP3, PTTG1, PRDM1, DGKQ, FCGR2A, IRAK1BP1, ITSN2 and PHIP, among oth
127 subsets characterized by high levels of PD1: Prdm1(+) effector regulatory T cells expressing immunore
131 , STAT1 directly regulates the expression of Prdm1 (encodes BLIMP-1) by binding to its promoter, and
132 lupus susceptibility genes such as IRF5 and PRDM1 (encoding for IFN regulatory factor 5 [IRF]5 and B
133 ssociated with decreased basal expression of PRDM1 (encoding PR domain containing 1, with ZNF domain)
134 Mice with a T cell-specific deletion of Prdm1, encoding Blimp-1, have aberrant T cell homeostasi
136 and functional characterization of zebrafish prdm1 exhibiting a dynamic and evolutionarily conserved
137 ion pressure with progressive elimination of PRDM1-expressing cells, which was enhanced when IL-2 con
138 an autoregulatory loop by which IL-2 induces Prdm1 expression and thus represses its own expression a
140 drugs may offer possibilities to reactivate PRDM1 expression as part of novel differentiation therap
141 hey in turn repress PRDM1, whereas prolonged PRDM1 expression inhibits neural, neural crest and senso
142 des BLIMP-1) by binding to its promoter, and Prdm1 expression is reduced in Stat1(-/-) MZ B cells.
145 tantly, we demonstrated that by upregulating PRDM1 expression, VLVs triggered differentiation signali
149 T(H)1/NK/ILC1 effector genes in LPLs, while Prdm1(fl/fl)Cd4(Cre) and Maf(fl/fl)Cd4(Cre) mice exhibit
152 an alternative mechanism of reducing normal PRDM1 function in a subset of DLBCL with relatively high
156 ECs, but not wild-type TECs, indicating that Prdm1 functions in TECs to regulate autoantibody product
157 m1 function by overexpression indicates that prdm1 functions to promote the cell fate specification o
158 STAT4, ATF4, TP63, EGR1, CDKN2A, RBL1, E2F1, PRDM1, GATA3, and IRF4) at 18 hours after exposure to E.
162 a novel BCL6 binding site on intron 3 of the PRDM1 gene, and show that BCL6 recruits MTA3 to this sit
167 the smyhc1-positive fibres express the ubo (prdm1) gene and adopt fast twitch fibre characteristics
170 controlling the expression of the Aicda and Prdm1 genes, which encode AID and Blimp-1, respectively.
175 of alternative mechanisms of down-regulating PRDM1 in a cohort of 25 primary DLBCL and six DLBCL cell
177 NA (crRNA) generates an exon3 skip mutant of PRDM1 in CAR-Ts, which leads to increased proliferation,
178 udy unveiled a novel regulatory mechanism of Prdm1 in cNK cells and liver ILC1s, showing promising po
179 t of mouse TECs, and conditional deletion of Prdm1 in either Keratin 14- or Foxn1-expressing cells in
181 GWAS, correlated with reduced expression of PRDM1 in ileal biopsy specimens and peripheral blood mon
183 e required for the BCR-induced expression of PRDM1 in lymphoma cells and in PU.1-positive myeloma cel
186 tumor suppressor gene, the reconstitution of PRDM1 in PRDM1-null NK cell lines led to G2/M cell cycle
190 identified clonal inactivating mutations in PRDM1 in the diffuse large B-cell lymphoma (DLBCL) cell
192 gene-exposure interaction that may implicate PRDM1 in the etiology of radiation therapy-induced SMNs.
193 ively, these data demonstrate a key role for PRDM1 in the negative regulation of NK activation and po
194 a crucial role for the transcription factor PRDM1 in the orderly transition from epiblast to defined
196 produced by keratinocytes after deletion of Prdm1 in vitro was mediated by the transcriptional activ
197 networks individually regulated by FOXP3 and PRDM1, in addition to a network coregulated by FOXO1 and
201 that FOXP1 directly represses expression of PRDM1, IRF4, and XBP1, transcriptional master regulators
202 iched for predicted binding sites for STAT6, PRDM1, IRF6, JDP2, NR2E1, and BCL6, suggesting a central
204 tro and in vivo experiments showed that that PRDM1 is a tumor suppressor gene in ALCL models, likely
207 rved; when the canonical B cell promoter for Prdm1 is deleted, differentiating B cells exhibit flexib
208 zinc finger transcriptional repressor Blimp1/PRDM1 is essential for the establishment of epithelial c
213 In sum, the transcriptional repressor Blimp1/Prdm1 is required for terminal differentiation of SpA-TG
215 hocyte-induced maturation protein 1 (BLIMP-1/PRDM1) is a master transcriptional repressor essential f
216 (PRDI-BF1-RIZ) domain zinc finger protein 1 (PRDM1) is a transcription repressor with a pivotal role
217 or fate determination, we found that Blimp1 (Prdm1) is expressed transiently in developing photorecep
227 oprecipitation (ChIP)-on-chip mapping of the PRDM1 locus, identifying a novel BCL6 binding site on in
229 scRNA-seq) data also provided evidences that Prdm1 maintains functional subsets of cNK cells and live
233 icantly expressed PRDM1 and TFAP2C, although PRDM1 mRNA in CD38(-) cells lacked the 3'-UTR harboring
234 d mutation, and conversely overexpression of prdm1 mRNA rescues the nrd RB sensory neuron and neural
235 gulating select miRNAs that target Aicda and Prdm1 mRNA-3'UTRs through inhibition of histone deacetyl
237 a Tbx1 heterozygote background, conditional Prdm1 mutants have more pronounced arterial pole defects
238 were identified in a subset of DLBCL without PRDM1 mutations, the primarily non-GCB type, consistent
239 oped anti-nuclear Abs when transplanted with Prdm1 null TECs, but not wild-type TECs, indicating that
240 pressor gene, the reconstitution of PRDM1 in PRDM1-null NK cell lines led to G2/M cell cycle arrest,
241 in LPLs from infected mice in the absence of Prdm1 or Maf, revealing potential mechanisms of human di
243 ecific interactions, like Pax5/Ebf1 vs. Pax5/Prdm1, or the role of different NF-kappaB dimers in diff
248 (B lymphocyte-induced maturation protein-1)/PRDM1 (PR domain-containing 1, with ZNF domain) binding
249 and butyrate dampened AICDA/Aicda (AID) and PRDM1/Prdm1 (Blimp-1) mRNAs by upregulating miR-155, miR
250 HM), and Bcl6, Bach2, or Pax5 (repressors of PRDM1/Prdm1 expression), as well as unchanged expression
251 ibitor-mediated silencing of AICDA/Aicda and PRDM1/Prdm1 was emphasized by unchanged expression of Ho
255 ession of key germline transcription factors Prdm1, Prdm14 and Tfap2c, directly induce PGC-like cells
256 ic expression of the germ line-related genes PRDM1, PRDM14, LIN28A, DAZL, VASA and SYCP3 induced dire
257 ethylation augments STAT3 association at the Prdm1 promoter and a downstream enhancer, thus ensuring
261 PRDM1 and VSX2 work in opposition, such that PRDM1 promotes photoreceptor fate and VSX2 bipolar cell
263 ed abundant mature EOMES(-) ILC1s expressing PRDM1 rather than ZNF683, alongside a few immature TCF7(
264 The zinc finger transcription factor Blimp1/PRDM1 regulates gene expression in diverse cell types.
265 the transcription factor Blimp-1 (encoded by Prdm1) repressed expression of the gene encoding catheps
269 ession of ERAP1, TAPASIN, MECL1, and LMP7 by PRDM1 results in failure to up-regulate surface MHC clas
270 -6) replication, P = 1 x 10(-9) overall) and PRDM1 (rs548234, P = 1 x 10(-5) replication, P = 2 x 10(
271 ic model where the evolutionary emergence of PRDM1-S and epigenetic priming of AP-1/IRF may be key dr
275 te that the pioneer TF FOXA coordinates with PRDM1 TF to recruit nucleosome remodeling and deacetylat
276 fied an IL-21 response element downstream of Prdm1 that binds the transcription factors STAT3 and IRF
277 n factors (e.g., Nfatc2, Fos, Jun, Ets1, and Prdm1) that are critical for PD-1 transcription, exubera
278 egulatory domain zinc finger protein 1 gene (PRDM1) that encodes the positive regulatory domain I bin
279 of PR domain containing 1, with ZNF domain (Prdm1), the gene encoding Blimp-1, in adult mice caused
281 ave identified two intronic regions of mouse prdm1, the gene encoding B lymphocyte-induced maturation
286 rtholog, we demonstrate that the capacity of PRDM1 to repress the IFN response of such promoters is e
287 red fluorescent protein, under regulation by Prdm1 transcriptional elements, and we achieved transduc
292 emonstrated that VLV-induced upregulation of PRDM1 was necessary and sufficient to reactivate KSHV by
295 nants become expressed, they in turn repress PRDM1, whereas prolonged PRDM1 expression inhibits neura
296 ed excess Bcl-6 to repress its direct target Prdm1 (which encodes the transcriptional repressor Blimp
297 transcription factor Blimp-1 (also known as Prdm1), which is a widely conserved bilaterian gene know
298 n of transcription factor BLIMP1 (encoded by Prdm1), which regulates plasma cell differentiation and
300 ivating transcription factors (GRHL3, OVOL1, PRDM1, ZNF750) to advance terminal differentiation.