| ZBTB24 (Zinc Finger and BTB Domain Containing 24) prevents recurrent spontaneous abortion by promoting trophoblast proliferation, differentiation and migration. | ZBTB24 (Zinc Finger and BTB Domain Containing 24) prevents recurrent spontaneous abortion by promoting trophoblast proliferation, differentiation and migration.
Ruan H, Dai Z, Yan J, Long X, Chen Y, Yang Y, Yang Q, Zhu J, Zheng M, Zhang X., Free PMC Article | 02/26/2022 |
| Loss of ZBTB24 impairs nonhomologous end-joining and class-switch recombination in patients with ICF syndrome. | Loss of ZBTB24 impairs nonhomologous end-joining and class-switch recombination in patients with ICF syndrome.
Helfricht A, Thijssen PE, Rother MB, Shah RG, Du L, Takada S, Rogier M, Moritz J, IJspeert H, Stoepker C, van Ostaijen-Ten Dam MM, Heyer V, Luijsterburg MS, de Groot A, Jak R, Grootaers G, Wang J, Rao P, Vertegaal ACO, van Tol MJD, Pan-Hammarström Q, Reina-San-Martin B, Shah GM, van der Burg M, van der Maarel SM, van Attikum H., Free PMC Article | 03/13/2021 |
| ZBTB24 activates the expression of CDCA7 in T cells.ZBTB24 regulates the apoptosis of T cells via CDCA7/TRAIL-R axis. | ZBTB24 regulates the apoptosis of human T cells via CDCA7/TRAIL-receptor axis.
Qin XY, Feng J, Chen G, Dou XW, Dai XQ, Dong HL, Gong FY, Xiao F, Zhao Y, Gao XM, Wang J. | 07/25/2020 |
| Identification of ZBTB24 protein domains and motifs for heterochromatin localization and transcriptional activation. Domains and motifs important for the biological function of ZBTB24, which provides a basis for understanding the molecular mechanisms underlying the pathogenesis of ICF syndrome. | Identification of ZBTB24 protein domains and motifs for heterochromatin localization and transcriptional activation.
Aktar S, Sasaki H, Unoki M. | 03/21/2020 |
| this study expands the clinical and mutation spectrum of Immunodeficiency, Centromeric Instability, and Facial Anomalies Syndrome by analyzing Saudi hypogammaglobulinemia patients and a novel deletion in the ZBTB24 gene | Three Types of Immunodeficiency, Centromeric Instability, and Facial Anomalies (ICF) Syndrome Identified by Whole-Exome Sequencing in Saudi Hypogammaglobulinemia Patients: Clinical, Molecular, and Cytogenetic Features.
Alghamdi HA, Tashkandi SA, Alidrissi EM, Aledielah RD, AlSaidi KA, Alharbi ES, Habazi MK, Alzahrani MS. | 10/5/2019 |
| Chromatin immunoprecipitation coupled with loss-of-function approaches in model systems revealed common loci bound by ZBTB24 and DNMT3B, where they function to regulate gene body methylation. Genes coordinately regulated by ZBTB24 and DNMT3B are enriched for molecular mechanisms essential for cellular homeostasis, highlighting the importance of the ZBTB24-DNMT3B interplay in maintaining epigenetic patterns | ZBTB24 is a transcriptional regulator that coordinates with DNMT3B to control DNA methylation.
Thompson JJ, Kaur R, Sosa CP, Lee JH, Kashiwagi K, Zhou D, Robertson KD., Free PMC Article | 06/29/2019 |
| in contrast to Immunodeficiency, Centromeric instability and Facial anomalies syndrome type 1 (ICF1), the subtelomeric methylation patterns in cells of ICF2-4 patients do not differ significantly from those in normal cells, and ICF2-4 cells exhibit a normal telomeric phenotype. Also knocking down the expression of ZBTB24, CDCA7 and HELLS in normal human fibroblasts does not affect subtelomeric methylation. | Subtelomeric methylation distinguishes between subtypes of Immunodeficiency, Centromeric instability and Facial anomalies syndrome.
Toubiana S, Velasco G, Chityat A, Kaindl AM, Hershtig N, Tzur-Gilat A, Francastel C, Selig S. | 05/25/2019 |
| Here, we performed a comparative analysis of perturbed DNA methylation landscapes in a cohort of ICF patients using an array-based assay to (i) evaluate the similarities and differences in methylation landscapes depending on patient genotypes as an index of a functional link between the four ICF factors, (ii) identify genomic regions that rely on DNMT3B, ZBTB24, CDCA7 or HELLS for their methylation status | Comparative methylome analysis of ICF patients identifies heterochromatin loci that require ZBTB24, CDCA7 and HELLS for their methylated state.
Velasco G, Grillo G, Touleimat N, Ferry L, Ivkovic I, Ribierre F, Deleuze JF, Chantalat S, Picard C, Francastel C. | 03/16/2019 |
| data indicate that SRRM4 regulates alternative RNA splicing of the Bif-1 gene that enables PCa cells resistant to apoptotic stimuli under anti-cancer therapies, and may contribute to AdPC progression into t-NEPC. | Roles of Alternative RNA Splicing of the Bif-1 Gene by SRRM4 During the Development of Treatment-induced Neuroendocrine Prostate Cancer.
Gan Y, Li Y, Long Z, Lee AR, Xie N, Lovnicki JM, Tang Y, Chen X, Huang J, Dong X., Free PMC Article | 09/29/2018 |
| The biallelic deletion of ZBTB24 provides strong support for the hypothesis that most ICF2 patients suffer from a ZBTB24 loss of function mechanism and confirms that complete absence of ZBTB24 is compatible with human life. This is in contrast to the observed early embryonic lethality in mice lacking functional Zbtb24 | Expanding the mutation spectrum in ICF syndrome: Evidence for a gender bias in ICF2.
van den Boogaard ML, Thijssen PE, Aytekin C, Licciardi F, Kıykım AA, Spossito L, Dalm VASH, Driessen GJ, Kersseboom R, de Vries F, van Ostaijen-Ten Dam MM, Ikinciogullari A, Dogu F, Oleastro M, Bailardo E, Daxinger L, Nain E, Baris S, van Tol MJD, Weemaes C, van der Maarel SM. | 05/19/2018 |
| Transcriptome analysis identified Cdca7 as the top down-regulated gene in Zbtb24 homozygous mutant mESCs, which can be restored by ectopic ZBTB24 expression. Finally, we show that this regulation is conserved between species and that CDCA7 levels are reduced in patients carrying ZBTB24 nonsense mutations | Converging disease genes in ICF syndrome: ZBTB24 controls expression of CDCA7 in mammals.
Wu H, Thijssen PE, de Klerk E, Vonk KK, Wang J, den Hamer B, Aytekin C, van der Maarel SM, Daxinger L. | 07/22/2017 |
| Downregulation of ZBTB24 increases the expression of IRF-4 and reduces b-cell proliferation. | Downregulation of ZBTB24 hampers the G0/1- to S-phase cell-cycle transition via upregulating the expression of IRF-4 in human B cells.
Liang J, Yan R, Chen G, Feng J, Wu WW, Ren W, Zhu C, Zhao Y, Gao XM, Wang J. | 05/20/2017 |
| Our results demonstrate a novel role of Bif-1 in hepatocellular carcinoma (HCC), in which Bif-1 promotes cell metastasis by regulating Cdc42 expression and activity. | Bif-1 promotes tumor cell migration and metastasis via Cdc42 expression and activity.
Zhang C, Liu F, Chen H, Li N, Luo Z, Guo W, Huang D, Tang S, Wang H, Cheng S, Li Z, Wang H. | 03/25/2017 |
| ICF2, caused by biallelic ZBTB24 gene mutations, is acknowledged primarily as an isolated B-cell defect. | Combined immunodeficiency develops with age in Immunodeficiency-centromeric instability-facial anomalies syndrome 2 (ICF2).
von Bernuth H, Ravindran E, Du H, Fröhler S, Strehl K, Krämer N, Issa-Jahns L, Amulic B, Ninnemann O, Xiao MS, Eirich K, Kölsch U, Hauptmann K, John R, Schindler D, Wahn V, Chen W, Kaindl AM., Free PMC Article | 02/13/2016 |
| This suggests that Bif-1 protein expression may be a useful prognostic marker in early-stage CRC | Stage-stratified analysis of prognostic significance of Bax-interacting factor-1 expression in resected colorectal cancer.
Ko YH, Cho YS, Won HS, An HJ, Sun DS, Hong SU, Park JH, Lee MA., Free PMC Article | 06/21/2014 |
| Clinical and genetic data of mutations in DNMT3B and ZBTB24 in patients with ICF syndrome, were compared. | Heterogeneous clinical presentation in ICF syndrome: correlation with underlying gene defects.
Weemaes CM, van Tol MJ, Wang J, van Ostaijen-ten Dam MM, van Eggermond MC, Thijssen PE, Aytekin C, Brunetti-Pierri N, van der Burg M, Graham Davies E, Ferster A, Furthner D, Gimelli G, Gennery A, Kloeckener-Gruissem B, Meyn S, Powell C, Reisli I, Schuetz C, Schulz A, Shugar A, van den Elsen PJ, van der Maarel SM., Free PMC Article | 05/10/2014 |
| We report three novel ZBTB24 mutations in Japanese and Cape Verdean type 2 ICF syndrome patients. | Three novel ZBTB24 mutations identified in Japanese and Cape Verdean type 2 ICF syndrome patients.
Nitta H, Unoki M, Ichiyanagi K, Kosho T, Shigemura T, Takahashi H, Velasco G, Francastel C, Picard C, Kubota T, Sasaki H. | 02/15/2014 |
| A novel deletion in the ZBTB24 gene was responsible for causing immunodeficiency, centromeric instability and facial anomalies syndrome type 2 in this family. | A novel deletion in ZBTB24 in a Lebanese family with immunodeficiency, centromeric instability, and facial anomalies syndrome type 2.
Chouery E, Abou-Ghoch J, Corbani S, El Ali N, Korban R, Salem N, Castro C, Klayme S, Azoury-Abou Rjeily M, Khoury-Matar R, Debo G, Germanos-Haddad M, Delague V, Lefranc G, Mégarbané A. | 03/23/2013 |
| These data indicate that ZBTB24 is involved in DNA methylation of juxtacentromeric DNA and in B cell development and/or B and T cell interactions. | Mutations in ZBTB24 are associated with immunodeficiency, centromeric instability, and facial anomalies syndrome type 2.
de Greef JC, Wang J, Balog J, den Dunnen JT, Frants RR, Straasheijm KR, Aytekin C, van der Burg M, Duprez L, Ferster A, Gennery AR, Gimelli G, Reisli I, Schuetz C, Schulz A, Smeets DFCM, Sznajer Y, Wijmenga C, van Eggermond MC, van Ostaijen-Ten Dam MM, Lankester AC, van Tol MJD, van den Elsen PJ, Weemaes CM, van der Maarel SM., Free PMC Article | 08/20/2011 |