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    Spib Spi-B transcription factor (Spi-1/PU.1 related) [ Mus musculus (house mouse) ]

    Gene ID: 272382, updated on 17-Aug-2021

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Opposing Roles for the Related ETS-Family Transcription Factors Spi-B and Spi-C in Regulating B Cell Differentiation and Function.

    Opposing Roles for the Related ETS-Family Transcription Factors Spi-B and Spi-C in Regulating B Cell Differentiation and Function.
    Laramée AS, Raczkowski H, Shao P, Batista C, Shukla D, Xu L, Haeryfar SMM, Tesfagiorgis Y, Kerfoot S, DeKoter R., Free PMC Article

    The mechanism of action of Spi-B in the transcriptional activation of the interferon-alpha4 gene.

    The mechanism of action of Spi-B in the transcriptional activation of the interferon-α4 gene.
    Miyazaki R, Saiga H, Kato T, Bakoshi T, Senba R, Shintani A, Suzuki M, Takao K, Sasaki I, Iizuka A, Sugiyama M, Iwami N, Fukuda-Ohta Y, Hemmi H, Tanaka T, Miyake M, Kaisho T, Hoshino K.

    Mice lacking both PU.1 and SpiB in mature B cells do not generate germinal centers and high-affinity antibody after protein immunization. PU.1 and SpiB double-deficient B cells have a survival defect after engagement of CD40 or Toll-like receptors (TLR), despite paradoxically enhanced plasma cell differentiation.

    Environmental sensing by mature B cells is controlled by the transcription factors PU.1 and SpiB.
    Willis SN, Tellier J, Liao Y, Trezise S, Light A, O'Donnell K, Garrett-Sinha LA, Shi W, Tarlinton DM, Nutt SL., Free PMC Article

    Mechanistic analysis indicated that E47 activated expression of the transcription factor Spi-B and the suppressor of cytokine signaling 3 (SOCS3), which both downregulated Foxp3 expression. These findings demonstrate that the balance of Id3 and E47 controls the maintenance of Foxp3 expression in Treg cells and, thus, contributes to Treg cell plasticity.

    Id3 Maintains Foxp3 Expression in Regulatory T Cells by Controlling a Transcriptional Network of E47, Spi-B, and SOCS3.
    Rauch KS, Hils M, Lupar E, Minguet S, Sigvardsson M, Rottenberg ME, Izcue A, Schachtrup C, Schachtrup K.

    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.

    Genome-wide comparison of PU.1 and Spi-B binding sites in a mouse B lymphoma cell line.
    Solomon LA, Li SK, Piskorz J, Xu LS, DeKoter RP., Free PMC Article

    Nfkb1 transcriptional activation by PU.1 and Spi-B promotes toll-like receptor-mediated B cell proliferation.

    Nfkb1 activation by the E26 transformation-specific transcription factors PU.1 and Spi-B promotes Toll-like receptor-mediated splenic B cell proliferation.
    Li SK, Abbas AK, Solomon LA, Groux GM, DeKoter RP., Free PMC Article

    Data show that transcription factor Spi-B-mediated negative feedback regulation limited medullary thymic epithelial cells (mTECs) development.

    Limitation of immune tolerance-inducing thymic epithelial cell development by Spi-B-mediated negative feedback regulation.
    Akiyama N, Shinzawa M, Miyauchi M, Yanai H, Tateishi R, Shimo Y, Ohshima D, Matsuo K, Sasaki I, Hoshino K, Wu G, Yagi S, Inoue J, Kaisho T, Akiyama T., Free PMC Article

    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.

    Transcription factor Spi-B-dependent and -independent pathways for the development of Peyer's patch M cells.
    Sato S, Kaneto S, Shibata N, Takahashi Y, Okura H, Yuki Y, Kunisawa J, Kiyono H.

    Data indicate that the developmental defects of plasmacytoid dendritic cells (pDC) in Spi-B-deficient mice were more prominent in the bone marrow.

    Spi-B is critical for plasmacytoid dendritic cell function and development.
    Sasaki I, Hoshino K, Sugiyama T, Yamazaki C, Yano T, Iizuka A, Hemmi H, Tanaka T, Saito M, Sugiyama M, Fukuda Y, Ohta T, Sato K, Ainai A, Suzuki T, Hasegawa H, Toyama-Sorimachi N, Kohara H, Nagasawa T, Kaisho T.

    The Blnk 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.

    Regulation of B cell linker protein transcription by PU.1 and Spi-B in murine B cell acute lymphoblastic leukemia.
    Xu LS, Sokalski KM, Hotke K, Christie DA, Zarnett O, Piskorz J, Thillainadesan G, Torchia J, DeKoter RP.

    RankL-induced expression of SpiB is essential for Lgr5 stem cell-derived epithelial precursors to develop into Peyer's patch M cells

    Peyer's patch M cells derived from Lgr5(+) stem cells require SpiB and are induced by RankL in cultured "miniguts".
    de Lau W, Kujala P, Schneeberger K, Middendorp S, Li VS, Barker N, Martens A, Hofhuis F, DeKoter RP, Peters PJ, Nieuwenhuis E, Clevers H., Free PMC Article

    Spi-B is an essential transcription factor that regulates M-cell differentiation.

    The Ets transcription factor Spi-B is essential for the differentiation of intestinal microfold cells.
    Kanaya T, Hase K, Takahashi D, Fukuda S, Hoshino K, Sasaki I, Hemmi H, Knoop KA, Kumar N, Sato M, Katsuno T, Yokosuka O, Toyooka K, Nakai K, Sakamoto A, Kitahara Y, Jinnohara T, McSorley SJ, Kaisho T, Williams IR, Ohno H., Free PMC Article

    Regulation of follicular B cell differentiation by the related E26 transformation-specific transcription factors PU.1, Spi-B, and Spi-C.

    Regulation of follicular B cell differentiation by the related E26 transformation-specific transcription factors PU.1, Spi-B, and Spi-C.
    DeKoter RP, Geadah M, Khoosal S, Xu LS, Thillainadesan G, Torchia J, Chin SS, Garrett-Sinha LA.

    Reduction of Spi-B activity in pro-B cells promotes their differentiation to a stage intermediate between late pro-B cells and large pre-B cells.

    Analysis of gene expression and Ig transcription in PU.1/Spi-B-deficient progenitor B cell lines.
    Schweitzer BL, DeKoter RP.

    Maintenance of the B-2 type cell phenotype requires relatively high levels of PU.1, but B-1 cells require little.

    PU.1 is not strictly required for B cell development and its absence induces a B-2 to B-1 cell switch.
    Ye M, Ermakova O, Graf T., Free PMC Article

    potential positive autoregulatory loop mediated through an upstream regulatory element is essential for proper PU.1 gene expression

    Potential autoregulation of transcription factor PU.1 by an upstream regulatory element.
    Okuno Y, Huang G, Rosenbauer F, Evans EK, Radomska HS, Iwasaki H, Akashi K, Moreau-Gachelin F, Li Y, Zhang P, Göttgens B, Tenen DG., Free PMC Article

    Spi-B function is necessary for efficient development of fetal thymocytes at the CD4-CD8-CD44-CD25+ (DN) checkpoint to the CD4+CD8+ (DP) stage; dysregulation of Spi-B expression results in a dose-dependent perturbation of thymocyte development.

    Enforced expression of Spi-B reverses T lineage commitment and blocks beta-selection.
    Lefebvre JM, Haks MC, Carleton MO, Rhodes M, Sinnathamby G, Simon MC, Eisenlohr LC, Garrett-Sinha LA, Wiest DL.

    The present findings establish a hierarchy between these two factors and provide a molecular link between OBF-1 and B cell receptor signaling.

    The Ets factor Spi-B is a direct critical target of the coactivator OBF-1.
    Bartholdy B, Du Roure C, Bordon A, Emslie D, Corcoran LM, Matthias P., Free PMC Article

    DNA microarray analyses enabled us to identify two genes inhibited by v-Abl that encode the Igk 3' enhancer-binding transcription factors Spi-B and IRF-4.

    A small molecule Abl kinase inhibitor induces differentiation of Abelson virus-transformed pre-B cell lines.
    Muljo SA, Schlissel MS.

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