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The protein encoded by SPIB is a transcriptional activator that binds to the PU-box (5'-GAGGAA-3') and acts as a lymphoid-specific enhancer. Zusätzlich bieten wir Ihnen SPIB Proteine (4) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal SPIB Primary Antibody für WB - ABIN1881823
Schmidlin, Diehl, Nagasawa, Scheeren, Schotte, Uittenbogaart, Spits, Blom: Spi-B inhibits human plasma cell differentiation by repressing BLIMP1 and XBP-1 expression. in Blood 2008
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Human Monoclonal SPIB Primary Antibody für ICC, FACS - ABIN1098113
Marshall, Dunham, Major: Transcription factor Spi-B binds unique sequences present in the tandem repeat promoter/enhancer of JC virus and supports viral activity. in The Journal of general virology 2010
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Mouse (Murine) Polyclonal SPIB Primary Antibody für CyTOF, FACS - ABIN4899321
Sehgal, Kobayashi, Donaldson, Mabbott: c-Rel is dispensable for the differentiation and functional maturation of M cells in the follicle-associated epithelium. in Immunobiology 2016
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Cow (Bovine) Polyclonal SPIB Primary Antibody für WB - ABIN2780475
Dontje, Schotte, Cupedo, Nagasawa, Scheeren, Gimeno, Spits, Blom: Delta-like1-induced Notch1 signaling regulates the human plasmacytoid dendritic cell versus T-cell lineage decision through control of GATA-3 and Spi-B. in Blood 2006
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spib is required for myeloid specification, and, in its absence, primitive myeloid cells retain hemangioblast-like characteristics and fail to migrate.
These results show that the mechanism of action of lenalidomide in ABC (zeige ABCB6 Antikörper)-DLBCL cells involves downregulation of SPIB transcription by cereblon (zeige CRBN Antikörper)-induced degradation of IKAROS (zeige IKZF1 Antikörper).
High SPIB expression is associated with Lung Cancer metastasis.
our data indicate that SPIB expression is a clinically novel poor prognostic factor in DLBCL that contributes to treatment resistance, at least in part, through an anti-apoptotic mechanism.
Findings establish a molecular hierarchy among POU2F2, SPIB and ID2 during B-cell differentiation, and suggest that aberrant expression of these transcription factors plays an important role in arresting plasmacytic differentiation in WM.
The SRC (zeige SRC Antikörper) family tyrosine kinase (zeige TXK Antikörper) HCK (zeige HCK Antikörper) and the ETS (zeige ETS1 Antikörper) family transcription factors SPIB and EHF (zeige EHF Antikörper) regulate transcytosis across a human follicle-associated epithelium model.
Our data indicate that the CBFbeta (zeige CBFB Antikörper)-SMMHC's C-terminus is essential to induce embryonic hematopoietic defects and leukemogenesis.
Fine mapping identified 26 single-nucleotide polymorphisms (SNPs) across the CLEC16A (zeige CLEC16A Antikörper)-SOCS1 (zeige SOCS1 Antikörper) and 11 SNPs across the SPIB locus with significant association to primary biliary cirrhosis.
Data show that in a cereblon (zeige CRBN Antikörper)-dependent fashion, lenalidomide downregulates IRF4 (zeige IRF4 Antikörper) and SPIB, transcription factors that together prevent IFNbeta production.
The transcription factor Spi-B regulates human plasmacytoid dendritic cell survival through direct induction of the antiapoptotic gene BCL2 (zeige BCL2 Antikörper)-A1.
The effect of mutating Spi-B-binding sites within the JC virus promoter/enhancer on early viral gene expression strongly suggests a role for Spi-B binding to the viral promoter/enhancer in the activation of early viral gene expression.
Mechanistic analysis indicated that E47 (zeige TCF3 Antikörper) activated expression of the transcription factor Spi-B and the suppressor of cytokine signaling 3 (SOCS3 (zeige SOCS3 Antikörper)), which both downregulated Foxp3 (zeige FOXP3 Antikörper) expression. These findings demonstrate that the balance of Id3 (zeige ID3 Antikörper) and E47 (zeige TCF3 Antikörper) controls the maintenance of Foxp3 (zeige FOXP3 Antikörper) expression in Treg cells and, thus, contributes to Treg cell plasticity.
Our results suggest that complementary biological functions of PU.1 and Spi-B may be explained by their interaction with a similar set of regions in the genome of B cells.
Nfkb1 (zeige NFKB1 Antikörper) transcriptional activation by PU.1 and Spi-B promotes toll (zeige TLR4 Antikörper)-like receptor-mediated B cell proliferation.
Data show that transcription factor Spi-B-mediated negative feedback regulation limited medullary thymic epithelial cells (mTECs) development.
there is a small M-cell population with developmental regulation that is Spi-B independent; however, Spi-B is probably a candidate master regulator of M-cell functional maturation and development by another pathway.
Data indicate that the developmental defects of plasmacytoid dendritic cells (pDC (zeige PDC Antikörper)) in Spi-B-deficient mice were more prominent in the bone marrow.
The Blnk (zeige BLNK Antikörper) promoter contains a predicted PU.1 and/or Spi-B binding site that is required for promoter activity and occupied by PU.1 and/or Spi-B.
RankL (zeige TNFSF11 Antikörper)-induced expression of SpiB is essential for Lgr5 (zeige LGR5 Antikörper) stem cell-derived epithelial precursors to develop into Peyer's patch M cells
Spi-B is an essential transcription factor that regulates M-cell differentiation.
Regulation of follicular B cell differentiation by the related E26 transformation-specific transcription factors PU.1, Spi-B, and Spi-C (zeige SPIC Antikörper).
The protein encoded by this gene is a transcriptional activator that binds to the PU-box (5'-GAGGAA-3') and acts as a lymphoid-specific enhancer. Four transcript variants encoding different isoforms have been found for this gene.
Spi-B transcription factor (Spi-1/PU.1 related) a
, transcription factor Spi-B
, Ets transcription factor Spi-B
, Spi-1/PU.1 related