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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

PR domain containing 1, with ZNF domain

Blimp-1, PRDM1, PRDI-BF1
This gene encodes a protein that acts as a repressor of beta-interferon gene expression. The protein binds specifically to the PRDI (positive regulatory domain I element) of the beta-IFN gene promoter. Transcription of this gene increases upon virus induction. Two alternatively spliced transcript variants that encode different isoforms have been reported. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: bcl-6, Qin, CAN, MUM1, RIZ1
Papers using Blimp-1 antibodies
Papers on Blimp-1
PEGylated siRNA lipoplexes for silencing of BLIMP-1 in Primary Effusion Lymphoma: In vitro evidences of antitumoral activity.
Ruozi et al., Reggio nell'Emilia, Italy. In Eur J Pharm Biopharm, Feb 2016
Silencing of the B lymphocyte-induced maturation protein 1 (Blimp-1), a pivotal transcriptional regulator during terminal differentiation of B cells into plasma cells with siRNAs is under investigation as novel therapeutic approach in Primary Effusion Lymphoma (PEL), a HHV-8 related and aggressive B cell Lymphoma currently lacking of an efficacious therapeutic approach.
NANOG alone induces germ cells in primed epiblast in vitro by activation of enhancers.
Azim Surani et al., Kōbe, Japan. In Nature, Feb 2016
Accordingly, we show that NANOG can bind and activate enhancers of Prdm1 and Prdm14 in EpiLCs in vitro; BLIMP1 (encoded by Prdm1) then directly induces Tfap2c.
Retrogenic ICOS Expression Increases Differentiation of KLRG-1hiCD127loCD8+ T Cells during Listeria Infection and Diminishes Recall Responses.
Ford et al., Atlanta, United States. In J Immunol, Feb 2016
Our results reveal that these ICOS signals critically impacted cell fate decisions of Ag-specific CD8(+) T cells, resulting in increased frequencies of KLRG-1(hi)CD127(lo) cells, altered BLIMP-1, T-bet, and eomesodermin expression, and increased cytolytic capacity as compared with empty vector controls.
NKG2D and CD28 receptors differentially activate mTOR to alter murine effector CD8(+) T cell differentiation.
Barber et al., United States. In Immunology, Jan 2016
Strong mTORc1 activation in CD28-costimulated cells also increased expression of transcription factors that support effector cell differentiation, namely T-bet, BLIMP1, IRF4, and ID2 whereas low levels of mTORc1 activation allowed for the expression of Eomes, BCL6, and ID3 during NKG2D stimulation, and increased expression of memory markers CD62L and CD127.
MYC-driven aggressive B-cell lymphomas: biology, entity, differential diagnosis and clinical management.
Young et al., Guangzhou, China. In Oncotarget, Dec 2015
One typical example is the failure of physiological repressors such as Bcl6 or BLIMP1 to suppress MYC over-expression.
Robust In Vitro Induction of Human Germ Cell Fate from Pluripotent Stem Cells.
Saitou et al., Kyoto, Japan. In Cell Stem Cell, Sep 2015
Accordingly, BLIMP1, which represses somatic programs in mice, activates and stabilizes a germline transcriptional circuit and represses a default neuronal differentiation program.
Transcriptional regulator PRDM12 is essential for human pain perception.
Senderek et al., Cambridge, United Kingdom. In Nat Genet, Jul 2015
Here we identified 10 different homozygous mutations in PRDM12 (encoding PRDI-BF1 and RIZ homology domain-containing protein 12) in subjects with CIP from 11 families.
A Unique Gene Regulatory Network Resets the Human Germline Epigenome for Development.
Surani et al., Cambridge, United Kingdom. In Cell, Jul 2015
This unique gene regulatory network, established by SOX17 and BLIMP1, drives comprehensive germline DNA demethylation by repressing DNA methylation pathways and activating TET-mediated hydroxymethylation.
Quantitative Dynamics of Chromatin Remodeling during Germ Cell Specification from Mouse Embryonic Stem Cells.
Saitou et al., Kyoto, Japan. In Cell Stem Cell, Jun 2015
T recruits H3K27ac to activate BLIMP1 and early mesodermal programs during PGCLC specification, which is followed by BLIMP1-mediated repression of a broad range of targets, possibly through recruitment and spreading of H3K27me3.
MYC alterations in diffuse large B-cell lymphomas.
Campo et al., Barcelona, Spain. In Semin Hematol, Apr 2015
BCL6 and BLIMP1 repress MYC expression in normal germinal center B and plasma cells, respectively.
Impact of MYC on malignant behavior.
Ott, Stuttgart, Germany. In Hematology Am Soc Hematol Educ Program, 2015
In the process of transformation, these secondary inhibitory functions of the MYC molecule have to be overcome through secondary mutations of the MYC gene itself and/or by abrogating the inhibitory effects of physiological regulators and/or repressors of proliferation such as BCL2, BCL6, BLIMP1, or others.
Primordial germ cell specification: a context-dependent cellular differentiation event [corrected].
Surani et al., Reykjavík, Iceland. In Philos Trans R Soc Lond B Biol Sci, 2015
While the majority of epiblast cells undergo differentiation towards somatic cell lineages, PGCs initiate a unique cellular programme driven by the cooperation of the transcription factors BLIMP1, PRDM14 and AP2γ.
Uncovering MicroRNA Regulatory Hubs that Modulate Plasma Cell Differentiation.
Lin et al., Taipei, Taiwan. In Sci Rep, 2014
Cohorts of differentially expressed miRNAs cooperating as miRNA hubs were predicted and validated to modulate key TFs, including a down-regulated miRNA hub containing miR-101-3p, -125b-5p, and -223-3p contributing to induction of PRDM1 as well as an up-regulated miRNA hub containing miR-34a-5p, -148a-3p, and -183-5p suppressing BCL6, BACH2, and FOXP1.
Genetic associations in classical hodgkin lymphoma: a systematic review and insights into susceptibility mechanisms.
Diepstra et al., Groningen, Netherlands. In Cancer Epidemiol Biomarkers Prev, 2014
PRDM1 is associated with radiation-induced secondary malignancies and a small number of genes are associated with treatment-related toxicities.
Genome-Wide Analysis Reveals Selective Modulation of microRNAs and mRNAs by Histone Deacetylase Inhibitor in B Cells Induced to Undergo Class-Switch DNA Recombination and Plasma Cell Differentiation.
Casali et al., San Antonio, United States. In Front Immunol, 2014
HDI repress the expression of AID and Blimp-1, which are critical for CSR/SHM and plasma cell differentiation, respectively, in mouse and human B cells by upregulating selected miRNAs that silenced AICDA/Aicda and PRDM1/Prdm1 mRNAs, as demonstrated by multiple qRT-PCRs (J Immunol 193:5933-5950, 2014).
Blimp1/Prdm1 governs terminal differentiation of endovascular trophoblast giant cells and defines multipotent progenitors in the developing placenta.
Robertson et al., Oxford, United Kingdom. In Genes Dev, 2012
the transcriptional repressor Blimp1/Prdm1 is required for terminal differentiation of endovascular trophoblast giant cells and defines a lineage-restricted progenitor cell population contributing to placental growth and morphogenesis
Alternative splicing regulates Prdm1/Blimp-1 DNA binding activities and corepressor interactions.
Bikoff et al., Oxford, United Kingdom. In Mol Cell Biol, 2012
Alternative splicing regulates Blimp-1 recruitment of corepressors and DNA binding activity.
Conditional inactivation of Blimp1 in adult mice promotes increased bone mass.
Miyamoto et al., Tokyo, Japan. In J Biol Chem, 2012
Conditional inactivation of Blimp1 inhibited osteoclast formation and increased bone mass in both male and female adult mice.
Activation of the Hippo pathway by CTLA-4 regulates the expression of Blimp-1 in the CD8+ T cell.
Fearon et al., London, United Kingdom. In Proc Natl Acad Sci U S A, 2012
The CTLA-4/Hippo pathway/Blimp-1 system may couple terminal differentiation of CD8(+) T cell with the magnitude of clonal expansion.
The germ cell determinant Blimp1 is not required for derivation of pluripotent stem cells.
Surani et al., Cambridge, United Kingdom. In Cell Stem Cell, 2012
Although Blimp1 is obligatory for primordial germ cell specification, it is not required for the reversion of epiblast stem cells to embryonic stem cells and for their maintenance thereafter.
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