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Validated All-in-One™ qPCR Primer for PRDM1(NM_001198.3) Search again
Product ID:
HQP109116
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BLIMP1, PRDI-BF1
Gene Description:
PR/SET domain 1
Target Gene Accession:
NM_001198.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
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].
Gene References into function
- were expressed by human PCs following a gradient of increasing maturity in the direction: tonsil-->blood-->BM
- Blimp-1 orchestrates plasma cell differentiation by extinguishing the mature B cell gene expression program
- BCL-6 regulates the Blimp-1 promoter through a novel mechanism involving AP-1 elements.
- Premature Blimp-1 expression coupled to altered and deficient Pax5 expression causes some proliferating B cells to prematurely differentiate to plasma cells in MM.
- PRDI-BF1 beta is abundantly expressed in myeloma cell lines through alternative transcription initiation, has a disrupted PR domain and a significantly impaired transcription repressor function on multiple target genes.
- PRDI-BF1 mediates silencing of interferon-beta gene transcription via recruitment of the histone H3 methyltransferase G9a.
- Transcriptional regulator PRD1-BF1 governing B-cell terminal cellular differentiation provides multiple myeloma- and other tumor- and nonmalignant-associated cytotoxic T-lymphocyte epitopes.
- identifies PRDM1 inactivation as a recurrent genetic defect in diffuse large B-cell lymphomas cells and establishes PRDM1 as a potential tumor suppressor gene.
- Blimp1 is a tumor suppressor gene, whose inactivation may contribute to lymphomagenesis by blocking post-germinal center differentiation of B cells toward plasma cells.
- tetanus toxoid (tet) (+) plasma cell (PC)expressed several times more positive regulatory domain I- binding factor 1/B lymphocyte-induced maturation protein 1 transcription factor than the tetC(-) PC
- diffuse large B-cell lymphoma cases with increased PRDM1 expression co-expressed BCL-6 and MUM1/IRF4, confirming that PRDM1 expression is insufficient to drive the full genetic program associated with plasmacytic differentiation
- In addition to silencing expression of major histocompatibility class II transactivator protein (CIITA) promoter III in B lymphocytes, PRDI-BF1 is capable of binding and suppressing CIITA promoter type IV.
- Results identify Viperin as a tightly regulated ISGF3 target gene, which is counter-regulated by PRDI-BF1.
- Normal human plasma cells have significantly lower levels of PRDI-BF1beta expression than plasma cells isolated from multiple myeloma patients.
- Altered expression of BLIMP1 may cause neoplastic B-cell proliferation; BLIMP1 is a pivotal molecule in the pathogenesis of diffuse large B-cell lymphoma.
- Suppression of p53 transcription is a crucial function of endogenous BLIMP1 and is essential for normal cell growth.
- both PRDM1alpha and PRDM1beta transcripts were expressed in microdissected lymphoma cells only in the non-germinal center B-cell-like (non-GCB) subtype of DLBCL
- Repression of PRDM1 by BSAP reveals an autoregulatory negative-feedback loop that could play a relevant role in controlling human PC differentiation.
- Blimp-1 expression is controlled by the same cgammaC cytokines that regulate T cell homeostasis suggesting a direct link between the extrinsic and intrinsic arms of the process.
- Blimp-1 ensures the survival of transformed plasma cells.
- that transcription factors Xbp-1, Blimp-1, and PAX-5-encoded BSAP play important roles in the regulation of plasmacytic differentiation and exert their effects on differentiation induced by low 2ME2 concentrations
- bortezomib down-regulation of PRDM1beta preceded decreased IRF4 and c-MYC expression
- reporter assays demonstrated that Bach2 and Bcl6 cooperate to repress Prdm1 through its intron enhancer region
- STAT3 activation functionally mimicked IL-21 treatment and that STAT3-mediated BLIMP1 up-regulation occurred despite high BCL6 expression levels
- In spite of some commonalities, different targets and regulators of Blimp-1 in B and T cells suggest intriguing evolutionary divergence of this regulatory machinery.
- By chromatin immunoprecipitation and assays using an inducible Spi-B construct BLIMP1 and XBP-1 were identified as direct target genes of Spi-B mediated repression.
- MiRNA-mediated down-regulation of PRDM1/Blimp-1 may contribute to the phenotype maintenance and pathogenesis of Hodgkin/Reed-Sternberg cells
- PRDM1 may be a tumor suppressor in some primary central nervous system lymphoma and contribute to lymphomagenesis by impairing terminal differentiation
- the basal activity of the human PRDM1 promoter, through which several factors, including SP1, SP3 and early growth response 1, modulate its expression through a conserved GC-box.
- Blimp-1Delta7 interferes with endogenous Blimp-1 expression, suggesting an auto-regulatory mechanism of Blimp-1 activation.