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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 nner in differentiating B cells and targeted Prdm1.
11 importance of Bcl-6-dependent repression of prdm1.
12 ntrolled, including GRHL3, ZNF750, KLF4, and PRDM1.
13 cis-regulatory elements, including those of Prdm1.
14 urthermore, we show that Blimp1 (also called Prdm1), a let-7 target and a master regulator of PGC spe
16 r responses triggered by VLVs and found that PRDM1, a master regulator in cell differentiation, was s
20 itch fibre characteristics in the absence of Prdm1 activity, whereas those that do not express smyhc1
24 by the activity of the transcription factor Prdm1 (also called Ubo or Blimp1) in response to Hedgeho
25 monstrate that the transcriptional repressor PRDM1 (also known as Blimp-1 or PRDI-BF1) is a critical
26 induction of PR domain-containing protein 1 (PRDM1; also known as Blimp-1), a critical regulator of p
30 ates that the functional interaction between PRDM1 and IFN-regulated pathways antedates the evolution
33 on-associated molecules such as Tim-3, Lag3, Prdm1 and Pbx3, and Bat3 knockdown in myelin-antigen-spe
34 hat NANOG can bind and activate enhancers of Prdm1 and Prdm14 in EpiLCs in vitro; BLIMP1 (encoded by
35 and CD38(-) EB cells significantly expressed PRDM1 and TFAP2C, although PRDM1 mRNA in CD38(-) cells l
37 noted as the PRDI-BF1 (HGMW-approved symbol PRDM1) and RIZ (HGMW-approved symbol PRDM2) homologous r
39 hese genes provide evidence that nfat5, fos, prdm1, and dusp16 are novel direct targets of Blimp-1.
40 Inducible, Cre-mediated deletion of Hspa5, Prdm1, and Xbp1 consistently induces cellular stress and
42 ive regulation of NK activation and position PRDM1 as a common regulator of the adaptive and innate i
43 nd the MHC, and identifies a unique role for PRDM1 as a key regulator of Ag presentation by MHC class
45 enetic defect in DLBCL cells and establishes PRDM1 as a potential tumor suppressor gene in DLBCL.
46 transcription factor binding motifs SRF and PRDM1 as important regulators of PIP3-sensitive mRNAs in
47 ified the transcriptional repressor Blimp-1 (PRDM1) as a downstream effector of the NF-kappaB, RelB/B
48 identified the transcription factor Blimp-1 (Prdm1) as a key IL-23-induced factor that drove the infl
49 n through the BCR rapidly induces endogenous PRDM1 at the level of transcription with minor changes i
52 domain containing 1 with zinc finger domain (PRDM1)/B lymphocyte-induced maturation protein 1 (BLIMP1
54 oma cell lines express the highest levels of PRDM1 beta mRNA relative to the full-length form, while
57 in LCLs inhibition of CDKN2C (p18INK4c) and PRDM1 (BLIMP-1) transcription results from direct bindin
61 Over-expression of miR-9 or let-7a reduced PRDM1/Blimp-1 levels in U266 cells by 30% to 50%, wherea
63 nding sites in the 3' untranslated region of PRDM1/blimp-1 mRNA and repressed luciferase reporter act
69 ube and colleagues have identified FOXO3 and PRDM1 (Blimp1) as tumor suppressor genes with a potentia
70 nd Igh enhancers and a distal element at the Prdm1 (Blimp1) locus, E-proteins contributed to Igk, Igh
71 AIOLOS), TBX21 (T-bet), NFIL3 (E4BP4), ZEB2, PRDM1 (BLIMP1), and RORA mRNA levels are higher in CD56(
73 ng the zinc finger transcriptional repressor Prdm1/Blimp1 (PR domain containing 1, with ZNF domain; p
74 at the zinc finger transcriptional repressor Prdm1/Blimp1 is essential for specification of spiral ar
76 misexpression and dominant-negative studies, Prdm1/Blimp1 was proposed to promote anterior endomesode
77 by the zinc finger transcriptional repressor Prdm1/Blimp1, an essential regulator of placenta develop
78 5b down-regulates the expression of IRF4 and PRDM1/BLIMP1, and memory B cell-enriched hsa-miR-223 dow
81 Thus, abnormal epigenetic down-regulation of PRDM1 by let-7 and other microRNAs may represent an alte
82 n experiments support a role of targeting of PRDM1 by microRNA let-7 family in mediating this down-re
84 dritic cell-specific conditional knockout of Prdm1 (CKO mice) altered the presentation of antigen to
86 inc-finger transcriptional repressor Blimp1 (Prdm1) controls gene expression patterns during differen
88 ine-specific deletion of Utf1 resulting from Prdm1-Cre mediated recombination are born with significa
89 neage tracing experiments exploiting a novel Prdm1.Cre-LacZ allele demonstrate that these Blimp1(+) c
92 29 other regions, including TNFAIP3, PTTG1, PRDM1, DGKQ, FCGR2A, IRAK1BP1, ITSN2 and PHIP, among oth
94 subsets characterized by high levels of PD1: Prdm1(+) effector regulatory T cells expressing immunore
98 , STAT1 directly regulates the expression of Prdm1 (encodes BLIMP-1) by binding to its promoter, and
99 lupus susceptibility genes such as IRF5 and PRDM1 (encoding for IFN regulatory factor 5 [IRF]5 and B
100 ssociated with decreased basal expression of PRDM1 (encoding PR domain containing 1, with ZNF domain)
101 Mice with a T cell-specific deletion of Prdm1, encoding Blimp-1, have aberrant T cell homeostasi
102 and functional characterization of zebrafish prdm1 exhibiting a dynamic and evolutionarily conserved
103 ion pressure with progressive elimination of PRDM1-expressing cells, which was enhanced when IL-2 con
104 an autoregulatory loop by which IL-2 induces Prdm1 expression and thus represses its own expression a
106 drugs may offer possibilities to reactivate PRDM1 expression as part of novel differentiation therap
107 des BLIMP-1) by binding to its promoter, and Prdm1 expression is reduced in Stat1(-/-) MZ B cells.
110 tantly, we demonstrated that by upregulating PRDM1 expression, VLVs triggered differentiation signali
114 an alternative mechanism of reducing normal PRDM1 function in a subset of DLBCL with relatively high
118 ECs, but not wild-type TECs, indicating that Prdm1 functions in TECs to regulate autoantibody product
119 m1 function by overexpression indicates that prdm1 functions to promote the cell fate specification o
123 a novel BCL6 binding site on intron 3 of the PRDM1 gene, and show that BCL6 recruits MTA3 to this sit
128 the smyhc1-positive fibres express the ubo (prdm1) gene and adopt fast twitch fibre characteristics
131 controlling the expression of the Aicda and Prdm1 genes, which encode AID and Blimp-1, respectively.
135 of alternative mechanisms of down-regulating PRDM1 in a cohort of 25 primary DLBCL and six DLBCL cell
136 t of mouse TECs, and conditional deletion of Prdm1 in either Keratin 14- or Foxn1-expressing cells in
137 GWAS, correlated with reduced expression of PRDM1 in ileal biopsy specimens and peripheral blood mon
139 e required for the BCR-induced expression of PRDM1 in lymphoma cells and in PU.1-positive myeloma cel
142 tumor suppressor gene, the reconstitution of PRDM1 in PRDM1-null NK cell lines led to G2/M cell cycle
146 identified clonal inactivating mutations in PRDM1 in the diffuse large B-cell lymphoma (DLBCL) cell
148 gene-exposure interaction that may implicate PRDM1 in the etiology of radiation therapy-induced SMNs.
149 ively, these data demonstrate a key role for PRDM1 in the negative regulation of NK activation and po
151 produced by keratinocytes after deletion of Prdm1 in vitro was mediated by the transcriptional activ
155 that FOXP1 directly represses expression of PRDM1, IRF4, and XBP1, transcriptional master regulators
157 tro and in vivo experiments showed that that PRDM1 is a tumor suppressor gene in ALCL models, likely
160 zinc finger transcriptional repressor Blimp1/PRDM1 is essential for the establishment of epithelial c
164 In sum, the transcriptional repressor Blimp1/Prdm1 is required for terminal differentiation of SpA-TG
165 (PRDI-BF1-RIZ) domain zinc finger protein 1 (PRDM1) is a transcription repressor with a pivotal role
166 or fate determination, we found that Blimp1 (Prdm1) is expressed transiently in developing photorecep
172 oprecipitation (ChIP)-on-chip mapping of the PRDM1 locus, identifying a novel BCL6 binding site on in
176 icantly expressed PRDM1 and TFAP2C, although PRDM1 mRNA in CD38(-) cells lacked the 3'-UTR harboring
177 d mutation, and conversely overexpression of prdm1 mRNA rescues the nrd RB sensory neuron and neural
179 a Tbx1 heterozygote background, conditional Prdm1 mutants have more pronounced arterial pole defects
180 were identified in a subset of DLBCL without PRDM1 mutations, the primarily non-GCB type, consistent
181 oped anti-nuclear Abs when transplanted with Prdm1 null TECs, but not wild-type TECs, indicating that
182 pressor gene, the reconstitution of PRDM1 in PRDM1-null NK cell lines led to G2/M cell cycle arrest,
186 (B lymphocyte-induced maturation protein-1)/PRDM1 (PR domain-containing 1, with ZNF domain) binding
187 and butyrate dampened AICDA/Aicda (AID) and PRDM1/Prdm1 (Blimp-1) mRNAs by upregulating miR-155, miR
188 HM), and Bcl6, Bach2, or Pax5 (repressors of PRDM1/Prdm1 expression), as well as unchanged expression
189 ibitor-mediated silencing of AICDA/Aicda and PRDM1/Prdm1 was emphasized by unchanged expression of Ho
192 ession of key germline transcription factors Prdm1, Prdm14 and Tfap2c, directly induce PGC-like cells
193 ic expression of the germ line-related genes PRDM1, PRDM14, LIN28A, DAZL, VASA and SYCP3 induced dire
198 the transcription factor Blimp-1 (encoded by Prdm1) repressed expression of the gene encoding catheps
202 ession of ERAP1, TAPASIN, MECL1, and LMP7 by PRDM1 results in failure to up-regulate surface MHC clas
203 -6) replication, P = 1 x 10(-9) overall) and PRDM1 (rs548234, P = 1 x 10(-5) replication, P = 2 x 10(
205 fied an IL-21 response element downstream of Prdm1 that binds the transcription factors STAT3 and IRF
206 egulatory domain zinc finger protein 1 gene (PRDM1) that encodes the positive regulatory domain I bin
207 of PR domain containing 1, with ZNF domain (Prdm1), the gene encoding Blimp-1, in adult mice caused
209 ave identified two intronic regions of mouse prdm1, the gene encoding B lymphocyte-induced maturation
214 rtholog, we demonstrate that the capacity of PRDM1 to repress the IFN response of such promoters is e
215 red fluorescent protein, under regulation by Prdm1 transcriptional elements, and we achieved transduc
219 emonstrated that VLV-induced upregulation of PRDM1 was necessary and sufficient to reactivate KSHV by
221 ed excess Bcl-6 to repress its direct target Prdm1 (which encodes the transcriptional repressor Blimp
222 transcription factor Blimp-1 (also known as Prdm1), which is a widely conserved bilaterian gene know
223 n of transcription factor BLIMP1 (encoded by Prdm1), which regulates plasma cell differentiation and
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