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Journal articles on the topic 'Zfhx1a'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Liu, Yongqing, Mary E. Costantino, Diego Montoya-Durango, Yujiro Higashi, Douglas S. Darling, and Douglas C. Dean. "The zinc finger transcription factor ZFHX1A is linked to cell proliferation by Rb–E2F1." Biochemical Journal 408, no. 1 (October 29, 2007): 79–85. http://dx.doi.org/10.1042/bj20070344.

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ZFHX1A is expressed in proliferating cells in the developing embryo, and in the present study we provide evidence that its expression is confined to proliferating cells through dependence on the Rb (retinoblastoma protein) family/E2F cell cycle pathway. Mutation of the Rb or E2F1 genes lead to induction of ZFHX1A mRNA, implying that the Rb–E2F1 repressor complex is important for repression of ZFHX1A. This repression is associated with recruitment of an E2F–Rb–histone deacetylase repressor complex to the promoter. A dominant-negative form of E2F1 inhibited ZFHX1A expression in p16INK4a(−) cells where Rb is constitutively hyperphosphorylated and inactive, suggesting that E2F can contribute to ZFHX1A transactivation in the absence of functional Rb. ZFHX1A is an E-box-binding transcription factor whose binding sites overlap with those bound by Snail1 and 2, and ZFHX1B/SIP1 (leading to at least partially overlapping function; for example, each of the proteins can repress E-cadherin expression). We found that expression of Snail1 and ZFHX1B/SIP1 is also regulated by E2Fs, but in contrast with ZFHX1A this regulation is Rb-family-independent. Snail2 expression was unaffected by either E2F or the Rb family. We propose that the differential effects of the Rb family/E2F pathway on expression of these E-box-binding proteins are important in maintaining their distinct patterns (and thus distinct functions) during embryogenesis.

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2

신정오, 정한성, 복진웅, and 이종민. "Expression patterns of Zfhx1a and Zfhx1b during mouse craniofacial development." Korean Journal of Oral Anatomy 39, no. 1 (December 2018): 1–8. http://dx.doi.org/10.35607/kjoa.39.1.201812.001.

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3

Kowase, Takanori, Heidi E. Walsh, Douglas S. Darling, and Margaret A. Shupnik. "Estrogen Enhances Gonadotropin-Releasing Hormone-Stimulated Transcription of the Luteinizing Hormone Subunit Promoters via Altered Expression of Stimulatory and Suppressive Transcription Factors." Endocrinology 148, no. 12 (December 1, 2007): 6083–91. http://dx.doi.org/10.1210/en.2007-0407.

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Transcription of the LH subunit genes is stimulated by GnRH and may be modulated physiologically by steroids such as 17β-estradiol (E). We found that E treatment amplified GnRH stimulation of the rat LHβ and α-subunit promoters, and expression of the endogenous mRNA, in LβT2 gonadotrope cells 2- to 5-fold above GnRH alone. We examined gene expression in LβT2 cells after E and/or GnRH treatment, and found that E suppressed expression of transcription factor Zfhx1a, and enhanced GnRH stimulation of Egr-1 mRNA and protein. E effects were abolished in the presence of antiestrogen. Egr-1 is critical for LHβ expression; however, the role of Zfhx1a, which binds to E-box sequences, was untested. We found E-box motifs in both the rat LHβ (−381, −182, and −15 bp) and α-subunit (−292, −64, −58 bp) promoters. Zfhx1a overexpression suppressed basal and GnRH-stimulated activity of both promoters. Mutation of the α-subunit promoter E boxes at either −64 or −58 bp eliminated Zfhx1a suppression, whereas mutation of the −292 bp E box had no effect. Gel shift assays demonstrated that Zfhx1a bound to the −64 and −58, but not −292, bp E-box DNA. Similarly, mutation of LHβ promoter E boxes at either −381 or −182, but not −15, bp reduced Zfhx1a suppression, correlating with binding of Zfhx1a. The −381 bp LHβ E box overlaps with an Sp1 binding site in the distal GnRH-stimulatory region, and increased Sp1 expression overcame Zfhx1a suppression. Thus, one mechanism by which E may enhance GnRH-stimulated LH subunit promoter activity is through regulation of both activators and suppressors of transcription.

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4

Tylzanowski, Przemko, Dirk De Valck, Vera Maes, Jenny Peeters, and Frank P. Luyten. "Zfhx1a and Zfhx1b mRNAs have non-overlapping expression domains during chick and mouse midgestation limb development." Gene Expression Patterns 3, no. 1 (March 2003): 39–42. http://dx.doi.org/10.1016/s1567-133x(02)00092-3.

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5

Manavella, Pablo A., Gonzalo Roqueiro, Douglas S. Darling, and Ana M. Cabanillas. "The ZFHX1A gene is differentially autoregulated by its isoforms." Biochemical and Biophysical Research Communications 360, no. 3 (August 2007): 621–26. http://dx.doi.org/10.1016/j.bbrc.2007.06.088.

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6

Gordon, M. S. "Hypoxia-Inducible Factor-1-Dependent Repression of E-cadherin in von Hippel-Lindau Tumor Suppressor—Null Renal Cell Carcinoma Mediated by TCF3, ZFHX1A, and ZFHX1B." Yearbook of Oncology 2007 (January 2007): 109–10. http://dx.doi.org/10.1016/s1040-1741(08)70352-x.

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7

Tylzanowski, Przemko, Dirk De Valck, Vera Maes, Jenny Peeters, and Frank P. Luyten. "Erratum to ‘Zfhx1a and Zfhx1b mRNAs have non-overlapping expression domains during chick and mouse midgestation limb development’ [Gene Expression Patterns 3 (2003) 39–42]." Gene Expression Patterns 3, no. 3 (June 2003): 383. http://dx.doi.org/10.1016/s1567-133x(03)00052-8.

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8

Krishnamachary, Balaji, David Zagzag, Hideko Nagasawa, Karin Rainey, Hiroaki Okuyama, Jin H. Baek, and Gregg L. Semenza. "Hypoxia-Inducible Factor-1-Dependent Repression of E-cadherin in von Hippel-Lindau Tumor Suppressor–Null Renal Cell Carcinoma Mediated by TCF3, ZFHX1A, and ZFHX1B." Cancer Research 66, no. 5 (March 1, 2006): 2725–31. http://dx.doi.org/10.1158/0008-5472.can-05-3719.

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9

Jin, Jiu-Zhen, Qun Li, Yujiro Higashi, Douglas S. Darling, and Jixiang Ding. "Analysis of Zfhx1a mutant mice reveals palatal shelf contact-independent medial edge epithelial differentiation during palate fusion." Cell and Tissue Research 333, no. 1 (May 10, 2008): 29–38. http://dx.doi.org/10.1007/s00441-008-0612-x.

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10

Anose, Bynthia M., and Michel M. Sanders. "Androgen Receptor Regulates Transcription of the ZEB1 Transcription Factor." International Journal of Endocrinology 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/903918.

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The zinc finger E-box binding protein 1 (ZEB1) transcription factor belongs to a two-member family of zinc-finger homeodomain proteins involved in physiological and pathological events mostly relating to cell migration and epithelial to mesenchymal transitions (EMTs). ZEB1 (also known as δEF1, zfhx1a, TCF8, and Zfhep) plays a key role in regulating such diverse processes as T-cell development, skeletal patterning, reproduction, and cancer cell metastasis. However, the factors that regulate its expression and consequently the signaling pathways in which ZEB1 participates are poorly defined. Because it is induced by estrogen and progesterone and is high in prostate cancer, we investigated whethertcf8, which encodes ZEB1, is regulated by androgen. Data herein demonstrate thattcf8is induced by dihydrotestosterone (DHT) in the human PC-3/AR prostate cancer cell line and that this induction is mediated by two androgen response elements (AREs). These results demonstrate that ZEB1 is an intermediary in androgen signaling pathways.

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11

Tang, Shu Min, Fen Fen Li, Shi Yao Lu, Ka Wai Kam, Pancy O. S. Tam, Clement C. Tham, Chi Pui Pang, Jason C. S. Yam, and Li Jia Chen. "Association of the ZC3H11B, ZFHX1B and SNTB1 genes with myopia of different severities." British Journal of Ophthalmology 104, no. 10 (July 12, 2019): 1472–76. http://dx.doi.org/10.1136/bjophthalmol-2019-314203.

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ObjectiveTo investigate the associations of single-nucleotide polymorphisms (SNPs) in the ZC3H11B, ZFHX1B, VIPR2, SNTB1 and MIPEP genes with severities of myopia in Chinese populations.MethodsBased on previous myopia genome-wide association studies, five SNPs (ZC3H11B rs4373767, ZFHX1B rs13382811, VIPR2 rs2730260, SNTB1 rs7839488 and MIPEP rs9318086) were selected for genotyping in a Chinese cohort of 2079 subjects: 252 extreme myopia, 277 high myopia, 393 moderate myopia, 366 mild myopia and 791 non-myopic controls. Genotyping was performed by TaqMan assays. Allelic frequencies of the SNPs were compared with myopia severities and ophthalmic biometric measurements.ResultsThe risk allele T of ZC3H11B SNP rs4373767 was significantly associated with high myopia (OR=1.39, p=0.007) and extreme myopia (OR=1.34, p=0.013) when compared with controls, whereas ZFHX1B rs13382811 (allele T, OR=1.33, p=0.018) and SNTB1 rs7839488 (allele G, OR=1.71, p=8.44E-05) were significantly associated with extreme myopia only. In contrast, there was no significant association of these SNPs with moderate or mild myopia. When compared with mild myopia, subjects carrying T allele of rs4373767 had a risk of progressing to high myopia (spherical equivalent ≤−6 dioptres) (OR=1.29, p=0.017). Similarly, the T allele of rs13382811 also imposed a significant risk to high myopia (OR=1.36, p=0.007). In quantitative traits analysis, SNPs rs4373767, rs13382811 and rs7839488 were correlated with axial length and refractive errors.ConclusionsWe confirmed ZC3H11B as a susceptibility gene for high and extreme myopia, and ZFHX1B and SNTB for extreme myopia in Chinese populations. Instead of myopia onset, these three genes were more likely to impose risks of progressing to high and extreme myopia.

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12

Christoffersen, N. R., A. Silahtaroglu, U. A. Orom, S. Kauppinen, and A. H. Lund. "miR-200b mediates post-transcriptional repression of ZFHX1B." RNA 13, no. 8 (June 29, 2007): 1172–78. http://dx.doi.org/10.1261/rna.586807.

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13

Dastot-Le Moal, Florence, Meredith Wilson, David Mowat, Nathalie Collot, Florence Niel, and Michel Goossens. "ZFHX1B mutations in patients with Mowat-Wilson syndrome." Human Mutation 28, no. 4 (2007): 313–21. http://dx.doi.org/10.1002/humu.20452.

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14

Dong, Ge, Gui Ma, Rui Wu, Jinming Liu, Mingcheng Liu, Ang Gao, Xiawei Li, et al. "ZFHX3 Promotes the Proliferation and Tumor Growth of ER-Positive Breast Cancer Cells Likely by Enhancing Stem-Like Features and MYC and TBX3 Transcription." Cancers 12, no. 11 (November 18, 2020): 3415. http://dx.doi.org/10.3390/cancers12113415.

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Breast cancer is a common malignancy, but the understanding of its cellular and molecular mechanisms is limited. ZFHX3, a transcription factor with many homeodomains and zinc fingers, suppresses prostatic carcinogenesis but promotes tumor growth of liver cancer cells. ZFHX3 regulates mammary epithelial cells’ proliferation and differentiation by interacting with estrogen and progesterone receptors, potent breast cancer regulators. However, whether ZFHX3 plays a role in breast carcinogenesis is unknown. Here, we found that ZFHX3 promoted the proliferation and tumor growth of breast cancer cells in culture and nude mice; and higher expression of ZFHX3 in human breast cancer specimens was associated with poorer prognosis. The knockdown of ZFHX3 in ZFHX3-high MCF-7 cells decreased, and ZFHX3 overexpression in ZFHX3-low T-47D cells increased the proportion of breast cancer stem cells (BCSCs) defined by mammosphere formation and the expression of CD44, CD24, and/or aldehyde dehydrogenase 1. Among several transcription factors that have been implicated in BCSCs, MYC and TBX3 were transcriptionally activated by ZFHX3 via promoter binding, as demonstrated by luciferase-reporter and ChIP assays. These findings suggest that ZFHX3 promotes breast cancer cells’ proliferation and tumor growth likely by enhancing BCSC features and upregulating MYC, TBX3, and others.

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15

Wu, Rui, Jiali Fang, Mingcheng Liu, Jun A, Jinming Liu, Wenxuan Chen, Juan Li, et al. "SUMOylation of the transcription factor ZFHX3 at Lys-2806 requires SAE1, UBC9, and PIAS2 and enhances its stability and function in cell proliferation." Journal of Biological Chemistry 295, no. 19 (April 5, 2020): 6741–53. http://dx.doi.org/10.1074/jbc.ra119.012338.

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SUMOylation is a posttranslational modification (PTM) at a lysine residue and is crucial for the proper functions of many proteins, particularly of transcription factors, in various biological processes. Zinc finger homeobox 3 (ZFHX3), also known as AT motif-binding factor 1 (ATBF1), is a large transcription factor that is active in multiple pathological processes, including atrial fibrillation and carcinogenesis, and in circadian regulation and development. We have previously demonstrated that ZFHX3 is SUMOylated at three or more lysine residues. Here, we investigated which enzymes regulate ZFHX3 SUMOylation and whether SUMOylation modulates ZFHX3 stability and function. We found that SUMO1, SUMO2, and SUMO3 each are conjugated to ZFHX3. Multiple lysine residues in ZFHX3 were SUMOylated, but Lys-2806 was the major SUMOylation site, and we also found that it is highly conserved among ZFHX3 orthologs from different animal species. Using molecular analyses, we identified the enzymes that mediate ZFHX3 SUMOylation; these included SUMO1-activating enzyme subunit 1 (SAE1), an E1-activating enzyme; SUMO-conjugating enzyme UBC9 (UBC9), an E2-conjugating enzyme; and protein inhibitor of activated STAT2 (PIAS2), an E3 ligase. Multiple analyses established that both SUMO-specific peptidase 1 (SENP1) and SENP2 deSUMOylate ZFHX3. SUMOylation at Lys-2806 enhanced ZFHX3 stability by interfering with its ubiquitination and proteasomal degradation. Functionally, Lys-2806 SUMOylation enabled ZFHX3-mediated cell proliferation and xenograft tumor growth of the MDA-MB-231 breast cancer cell line. These findings reveal the enzymes involved in, and the functional consequences of, ZFHX3 SUMOylation, insights that may help shed light on ZFHX3's roles in various cellular and pathophysiological processes.

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16

Kondybayeva, A. М., A. N. Akimniyazova, S. U. Kamenova, and A. Т. Ivashchenko. "THE CHARACTERISTICS OF MIRNA BINDING SITES IN MRNA OF ZFHX3 GENE AND ITS ORTHOLOGS." Vavilov Journal of Genetics and Breeding 22, no. 4 (July 3, 2018): 438–44. http://dx.doi.org/10.18699/vj18.380.

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Transcription factor gene ZFHX3 is one of the candidate genes involved in stroke development. The ZFHX3 protein contains oligopeptides encoded by trinucleotide repeats (TNRs). TNR variability is considered to be one of the causes of the disease, but their biological function has not yet been established. We assume that TNRs are the binding sites of miRNA to mRNA and are involved in regulation of ZFHX3 gene expression. The characteristics of miRNA–mRNA interaction were determined using MirTarget software. It has been shown that the first TNR in mRNA of the human ZFHX3 gene consists of the seven consecutive miR-12-32603-3p binding encoding polyGlu. The ZFHX3 protein of human polyGlu contains 30 Glu. In the orthologous proteins of 36 animal species the length of polyGlu varied from 27 Glu to 33 Glu. Negatively charged polyGlu of the ZFHX3 transcription factor probably interacted with positive DNA-binding proteins. The following mRNA region of the ZFHX3 gene contained the binding sites for miR-17-39416-3p, miR-5-15733-3p, miR-9-20317-3 encoding polyAla by 15 Ala lengths. In the 33 ZFHX3 orthologous proteins polyAla had the same length. The mRNA region of the human ZFHX3 gene with binding polysite of miR-1322-3p encoded polyGln consisting of 19 Gln. In the 41 orthologs of the ZFHX3 protein the length of polyGln varied from seven Gln to 23 Gln. The binding sites of miR-2-6184-3p, miR-5-14114-5p and miR-19-43437-5p were located with overlapping nucleotides sequences, and encode polyPro. In ZFHX3 human polyPro consisted of 12 Pro. In the orthologs, polyPro contained from 10 Pro to 14 Pro. The binding sites of miR-17-39416-3p, miR-9-20317-3p, miR-1-1819-3p, miR-5-15733-3p, miR-6-17815-3p, miR-18-39953-5p, miR-26862-5p, miR-1260b and miR-X-48174-3p in human ZFHX3 encoded polyGly by 22 Gly length. In the 28 orthologs of ZFHX3 the length of polyGly decreased to 11 Gly. The TNR regions could simultaneously bind several miRNAs, which increased the dependence of gene expression on miRNA. The oligopeptides encoded by the binding polysites of miRNA in mRNA in the orthologous ZFHX3 proteins were flanked by conserved oligopeptides.

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17

Fu, Changying, Na An, Jinming Liu, Jun A., Baotong Zhang, Mingcheng Liu, Zhiqian Zhang, et al. "The transcription factor ZFHX3 is crucial for the angiogenic function of hypoxia-inducible factor 1α in liver cancer cells." Journal of Biological Chemistry 295, no. 20 (April 10, 2020): 7060–74. http://dx.doi.org/10.1074/jbc.ra119.012131.

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Angiogenesis is a hallmark of tumorigenesis, and hepatocellular carcinoma (HCC) is hypervascular and therefore very dependent on angiogenesis for tumor development and progression. Findings from previous studies suggest that in HCC cells, hypoxia-induced factor 1α (HIF1A) and zinc finger homeobox 3 (ZFHX3) transcription factors functionally interact in the regulation of genes in HCC cells. Here, we report that hypoxia increases the transcription of the ZFHX3 gene and enhances the binding of HIF1A to the ZFHX3 promoter in the HCC cell lines HepG2 and Huh-7. Moreover, ZFHX3, in turn, physically associated with and was functionally indispensable for HIF1A to exert its angiogenic activity, as indicated by in vitro migration and tube formation assays of human umbilical vein endothelial cells (HUVECs) and microvessel formation in xenograft tumors of HCC cells. Mechanistically, ZFHX3 was required for HIF1A to transcriptionally activate the vascular endothelial growth factor A (VEGFA) gene by binding to its promoter. Functionally, down-regulation of ZFHX3 in HCC cells slowed their tumor growth, and addition of VEGFA to conditioned medium from ZFHX3-silenced HCC cells partially rescued the inhibitory effect of this medium on HUVEC tube formation. In human HCC, ZFHX3 expression was up-regulated, and this up-regulation correlated with both HIF1A up-regulation and worse patient survival, confirming a functional association between ZFHX3 and HIF1A in human HCC. We conclude that ZFHX3 is an angiogenic transcription factor that is integral to the HIF1A/VEGFA signaling axis in HCC cells.

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Galdieri, Luciano, Mitchell Grinwald, Zibi Gugala, Edward Oates, and Milan Chheda. "STEM-13. FUNCTIONAL CHARACTERIZATION OF THE ZFHX4-CHD4 INTERACTION IN GLIOBLASTOMA CANCER STEM CELLS." Neuro-Oncology 22, Supplement_2 (November 2020): ii199. http://dx.doi.org/10.1093/neuonc/noaa215.830.

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Abstract Glioblastoma stem cells (GSCs) they may be one reason for inevitable recurrence of GBM. We previously discovered that Zinc Finger Homeobox 4 (ZFHX4), a 450kD transcription factor, is required to maintain the GSC state. ZFHX4 interacts with CHD4, a core member of the nucleosome remodeling and deacetylase (NuRD) complex, which activates or represses gene expression via two distinct functions - histone deacetylation and ATP-dependent chromatin remodeling. CHD4 suppression phenocopies ZFHX4 suppression. The precise nature and function of the ZFHX4 interaction with CHD4 is not understood. Here we report that the ZFHX4-CHD4 interaction requires a single zinc-finger domain. An incremental truncation screen revealed that ZFHX4 amino acids 1838 to 2387, which contains zinc fingers 14 and 15, are required to bind CHD4. Disrupting the zinc coordination of zinc finger 14 impaired the ZFHX4-CHD4 interaction. Moreover, by overexpressing ZFHX4 amino acids 1838 to 2487, we decreased CHD4 recruitment to transcription regulatory regions of the stem cell genes SOX2 and SOX9, decreased transcription, and reduced clonogenic self-renewal. These results may provide the structural basis for new treatments to target GSCs and prevent recurrence in this devastating disease.

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Grabitz, Abby L., and Melinda K. Duncan. "Focus on Molecules: Smad Interacting Protein 1 (Sip1, ZEB2, ZFHX1B)." Experimental Eye Research 101 (August 2012): 105–6. http://dx.doi.org/10.1016/j.exer.2010.09.010.

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20

Wilcox, Ashleigh G., Lucie Vizor, Michael J. Parsons, Gareth Banks, and Patrick M. Nolan. "Inducible Knockout of Mouse Zfhx3 Emphasizes Its Key Role in Setting the Pace and Amplitude of the Adult Circadian Clock." Journal of Biological Rhythms 32, no. 5 (August 17, 2017): 433–43. http://dx.doi.org/10.1177/0748730417722631.

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The transcription factor zinc finger homeobox 3 (ZFHX3) plays a key role in coupling intracellular transcriptional-translational oscillations with intercellular synchrony in mouse suprachiasmatic nucleus (SCN). However, like many key players in central nervous system function, ZFHX3 serves an important role in neurulation and neuronal terminal differentiation while retaining discrete additional functions in the adult SCN. Recently, using a dominant missense mutation in mouse Zfhx3, we established that this gene can modify circadian period and sleep in adult animals. Nevertheless, we were still concerned that the neurodevelopmental consequences of ZFHX3 dysfunction in this mutant may interfere with, or confound, its critical adult-specific roles in SCN circadian function. To circumvent the developmental consequences of Zfhx3 deletion, we crossed a conditional null Zfhx3 mutant to an inducible, ubiquitously expressed Cre line (B6.Cg-Tg(UBC-cre/ERT2)1Ejb/J). This enabled us to assess circadian behavior in the same adult animals both before and after Cre-mediated excision of the critical Zfhx3 exons using tamoxifen treatment. Remarkably, we found a strong and significant alteration in circadian behavior in tamoxifen-treated homozygous animals with no phenotypic changes in heterozygous or control animals. Cre-mediated excision of Zfhx3 critical exons in adult animals resulted in shortening of the period of wheel-running in constant darkness by more than 1 h in the majority of homozygotes while, in 30% of animals, excision resulted in complete behavioral arrhythmicity. In addition, we found that homozygous animals reentrain almost immediately to 6-h phase advances in the light-dark cycle. No additional overt phenotypic changes were evident in treated homozygous animals. These findings confirm a sustained and significant role for ZFHX3 in maintaining rhythmicity in the adult mammalian circadian system.

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21

Perrella, Giorgio, Mhairi L. H. Davidson, Liz O’Donnell, Ana-Marie Nastase, Pawel Herzyk, Ghislain Breton, Jose L. Pruneda-Paz, Steve A. Kay, Joanne Chory, and Eirini Kaiserli. "ZINC-FINGER interactions mediate transcriptional regulation of hypocotyl growth in Arabidopsis." Proceedings of the National Academy of Sciences 115, no. 19 (April 23, 2018): E4503—E4511. http://dx.doi.org/10.1073/pnas.1718099115.

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Integration of environmental signals and interactions among photoreceptors and transcriptional regulators is key in shaping plant development. TANDEM ZINC-FINGER PLUS3 (TZP) is an integrator of light and photoperiodic signaling that promotes flowering in Arabidopsis thaliana. Here we elucidate the molecular role of TZP as a positive regulator of hypocotyl elongation. We identify an interacting partner for TZP, the transcription factor ZINC-FINGER HOMEODOMAIN 10 (ZFHD10), and characterize its function in coregulating the expression of blue-light–dependent transcriptional regulators and growth-promoting genes. By employing a genome-wide approach, we reveal that ZFHD10 and TZP coassociate with promoter targets enriched in light-regulated elements. Furthermore, using a targeted approach, we show that ZFHD10 recruits TZP to the promoters of key coregulated genes. Our findings not only unveil the mechanism of TZP action in promoting hypocotyl elongation at the transcriptional level but also assign a function to an uncharacterized member of the ZFHD transcription factor family in promoting plant growth.

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Stanchina, Laure, Tom Van de Putte, Michel Goossens, Danny Huylebroeck, and Nadege Bondurand. "Genetic interaction between Sox10 and Zfhx1b during enteric nervous system development." Developmental Biology 341, no. 2 (May 2010): 416–28. http://dx.doi.org/10.1016/j.ydbio.2010.02.036.

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23

Khor, Chiea Chuen, Masahiro Miyake, Li Jia Chen, Yi Shi, Veluchamy A. Barathi, Fan Qiao, Isao Nakata, et al. "Genome-wide association study identifies ZFHX1B as a susceptibility locus for severe myopia." Human Molecular Genetics 22, no. 25 (August 9, 2013): 5288–94. http://dx.doi.org/10.1093/hmg/ddt385.

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Dang, Lan T. H., Loksum Wong, and Vincent Tropepe. "Zfhx1b Induces a Definitive Neural Stem Cell Fate in Mouse Embryonic Stem Cells." Stem Cells and Development 21, no. 15 (October 10, 2012): 2838–51. http://dx.doi.org/10.1089/scd.2011.0593.

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25

Yoneda, M., T. Fujita, Y. Yamada, K. Yamada, A. Fujii, T. Inagaki, H. Nakagawa, et al. "Late infantile Hirschsprung disease-mental retardation syndrome with a 3-bp deletion in ZFHX1B." Neurology 59, no. 10 (November 26, 2002): 1637–40. http://dx.doi.org/10.1212/01.wnl.0000034842.78350.4e.

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26

Zweier, C. "Characterisation of deletions of the ZFHX1B region and genotype-phenotype analysis in Mowat-Wilson syndrome." Journal of Medical Genetics 40, no. 8 (August 1, 2003): 601–5. http://dx.doi.org/10.1136/jmg.40.8.601.

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27

Arbuzova, E. E., N. V. Selyanina, and A. V. Krivtsov. "INFLUENCE OF SINGLE NUCLEOTIDE POLYMORPHISMS OF “ZINC FINGERS” PROTEINS GENES ON MULTIPLE SCLEROSIS." Russian neurological Journal, no. 3 (September 3, 2019): 19–23. http://dx.doi.org/10.30629/2658-7947-2019-24-3-19-23.

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The genes ZFAT and ZFHX4 encoding the zinc finger proteins were previously identified as predisposing to autoimmune pathology and various cancer diseases, as well as influencing on therapeutic effect of interferonbeta in patients with multiple sclerosis. The aim of the study is to determine the associations of single nucleotide polymorphisms rs11787532 ZFHX4 and rs733254 ZFAT and development and severity of clinical manifestations of multiple sclerosis in Perm krai. A significant predominance of the C/A genotype of rs733254 ZFAT gene, and GC and CC haplotypes in people with multiple sclerosis was found. The association of single nucleotide polymorphisms with the severity of clinical manifestations of multiple sclerosis was not detected.

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van den Berghe, Veronique, André Goffinet, Rüdiger Klein, Nicoletta Kessaris, Kenneth Campbell, Danny Huylebroeck, and Eve Seuntjens. "20-P016 Smad-interacting protein-1 (Sip1/Zfhx1b) is crucial for tangential migration of gabaergic interneurons." Mechanisms of Development 126 (August 2009): S309. http://dx.doi.org/10.1016/j.mod.2009.06.849.

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29

Komine, Yuriko, Keizo Takao, Tsuyoshi Miyakawa, and Tetsuo Yamamori. "Behavioral Abnormalities Observed in Zfhx2-Deficient Mice." PLoS ONE 7, no. 12 (December 31, 2012): e53114. http://dx.doi.org/10.1371/journal.pone.0053114.

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Epifanova, Ekaterina, Valentina Salina, Denis Lajkó, Kathrin Textoris-Taube, Thomas Naumann, Olga Bormuth, Ingo Bormuth, et al. "Adhesion dynamics in the neocortex determine the start of migration and the post-migratory orientation of neurons." Science Advances 7, no. 27 (July 2021): eabf1973. http://dx.doi.org/10.1126/sciadv.abf1973.

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The neocortex is stereotypically organized into layers of excitatory neurons arranged in a precise parallel orientation. Here we show that dynamic adhesion both preceding and following radial migration is essential for this organization. Neuronal adhesion is regulated by the Mowat-Wilson syndrome-associated transcription factor Zeb2 (Sip1/Zfhx1b) through direct repression of independent adhesion pathways controlled by Neuropilin-1 (Nrp1) and Cadherin-6 (Cdh6). We reveal that to initiate radial migration, neurons must first suppress adhesion to the extracellular matrix. Zeb2 regulates the multipolar stage by transcriptional repression of Nrp1 and thereby downstream inhibition of integrin signaling. Upon completion of migration, neurons undergo an orientation process that is independent of migration. The parallel organization of neurons within the neocortex is controlled by Cdh6 through atypical regulation of integrin signaling via its RGD motif. Our data shed light on the mechanisms that regulate initiation of radial migration and the postmigratory orientation of neurons during neocortical development.

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Wu, Xiaoman, Fan Xiong, Hong Fang, Jie Zhang, and Mingxian Chang. "Crosstalks between NOD1 and Histone H2A Contribute to Host Defense against Streptococcus agalactiae Infection in Zebrafish." Antibiotics 10, no. 7 (July 15, 2021): 861. http://dx.doi.org/10.3390/antibiotics10070861.

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Correlation studies about NOD1 and histones have not been reported. In the present study, we report the functional correlation between NOD1 and the histone H2A variant in response to Streptococcus agalactiae infection. In zebrafish, NOD1 deficiency significantly promoted S. agalactiae proliferation and decreased larval survival. Transcriptome analysis revealed that the significantly enriched pathways in NOD1−/− adult zebrafish were mainly involved in immune and metabolism. Among 719 immunity-associated DEGs at 48 hpi, 74 DEGs regulated by NOD1 deficiency were histone variants. Weighted gene co-expression network analysis identified that H2A, H2B, and H3 had significant associations with NOD1 deficiency. Above all, S. agalactiae infection could induce the expression of intracellular histone H2A, as well as NOD1 colocalized with histone H2A, both in the cytoplasm and cell nucleus in the case of S. agalactiae infection. The overexpression of H2A variants such as zfH2A-6 protected against S. agalactiae infection and could improve cell survival in NOD1-deficient cells. Furthermore, NOD1 could interact with zfH2A-6 and cooperate with zfH2A-6 to inhibit the proliferation of S. agalactiae. NOD1 also showed a synergetic effect in inducing the expression of many antibacterial genes, especially antibacterial pattern recognition receptors PGRP2, PGRP5, and PGRP6. Collectively, these results firstly highlight the roles of NOD1 deficiency in the regulation of immune-related and metabolic pathways, and the correlation between zebrafish NOD1 and histone H2A variant in the defense against S. agalactiae infection.

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Nelles, Luc, Tom Van de Putte, Leo van Grunsven, Danny Huylebroeck, and Kristin Verschueren. "Organization of the mouse Zfhx1b gene encoding the two-handed zinc finger repressor Smad-interacting protein-1☆." Genomics 82, no. 4 (October 2003): 460–69. http://dx.doi.org/10.1016/s0888-7543(03)00169-1.

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Seuntjens, Eve, Anjana Nityanandam, Amaya Miquelajauregui, Joke Debruyn, Agata Stryjewska, Sandra Goebbels, Klaus-Armin Nave, Victor Tarabykin, and Danny Huylebroeck. "13-P024 Sip1 (Zfhx1b) regulates sequential fate decisions through feedback signaling from postmitotic neurons to progenitor cells." Mechanisms of Development 126 (August 2009): S202. http://dx.doi.org/10.1016/j.mod.2009.06.497.

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Ishihara, N. "Clinical and molecular analysis of Mowat-Wilson syndrome associated with ZFHX1B mutations and deletions at 2q22-q24.1." Journal of Medical Genetics 41, no. 5 (May 1, 2004): 387–93. http://dx.doi.org/10.1136/jmg.2003.016154.

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Komine, Yuriko, Keizo Takao, Tsuyoshi Miyakawa, and Tetsuo Yamamori. "Behavioral abnormalities caused by Zfhx2 deletion in mice." Neuroscience Research 65 (January 2009): S227. http://dx.doi.org/10.1016/j.neures.2009.09.1274.

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Cuturilo, Goran, Igor Stefanovic, Ida Jovanovic, Slobodanka Miletic-Grkovic, and Ivana Novakovic. "Mowat-Wilson syndrome: A case report." Srpski arhiv za celokupno lekarstvo 137, no. 7-8 (2009): 426–29. http://dx.doi.org/10.2298/sarh0908426c.

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Introduction. Mowat-Wilson syndrome (MWS) is characterised by severe mental retardation and multiple congenital anomalies. Key features for diagnosis are specific facial dysmorphism with uplifted ear lobes and Hirschsprung's disease. Ganglionic disorders of the colon, both the number of ganglion cells and the length of the aganglionic segment vary significantly in these patients. The disease is caused by ZFHX1B gene mutation. The management of MWS is symptomatic. Case outline. We report a four-year old boy with mental retardation, specific facial dysmorphy and multiple anomalies. During prenatal follow-up intrauterine growth retardation was revealed. Karyotype was normal. Clinical findings showed that growth and mental retardation, gastrointestinal disturbance and heart defect were predominant. A gastrostoma was inserted. Hypoganglionosis of the colon caused severe obstipation. He had a severe stenosis of the pulmonary artery and was a candidate for cardiac surgery. There were several attempts to establish diagnosis, but so far, without results. Conclusion. Hirschsprung's disease/hypoganglionosis of the colon associated with other congenital anomalies or mental retardation require evaluation for dysmorphic syndromes. One of them is MWS, presented in this report.

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Di Filippo, Ester Sara, Domiziana Costamagna, Giorgia Giacomazzi, Álvaro Cortés-Calabuig, Agata Stryjewska, Danny Huylebroeck, Stefania Fulle, and Maurilio Sampaolesi. "Zeb2 Regulates Myogenic Differentiation in Pluripotent Stem Cells." International Journal of Molecular Sciences 21, no. 7 (April 5, 2020): 2525. http://dx.doi.org/10.3390/ijms21072525.

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Skeletal muscle differentiation is triggered by a unique family of myogenic basic helix-loop-helix transcription factors, including MyoD, MRF-4, Myf-5, and Myogenin. These transcription factors bind promoters and distant regulatory regions, including E-box elements, of genes whose expression is restricted to muscle cells. Other E-box binding zinc finger proteins target the same DNA response elements, however, their function in muscle development and regeneration is still unknown. Here, we show that the transcription factor zinc finger E-box-binding homeobox 2 (Zeb2, Sip-1, Zfhx1b) is present in skeletal muscle tissues. We investigate the role of Zeb2 in skeletal muscle differentiation using genetic tools and transgenic mouse embryonic stem cells, together with single-cell RNA-sequencing and in vivo muscle engraftment capability. We show that Zeb2 over-expression has a positive impact on skeletal muscle differentiation in pluripotent stem cells and adult myogenic progenitors. We therefore propose that Zeb2 is a novel myogenic regulator and a possible target for improving skeletal muscle regeneration. The non-neural roles of Zeb2 are poorly understood.

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McKinsey, Gabriel L., Susan Lindtner, Brett Trzcinski, Axel Visel, Len A. Pennacchio, Danny Huylebroeck, Yujiro Higashi, and John L. R. Rubenstein. "Dlx1&2-Dependent Expression of Zfhx1b (Sip1, Zeb2) Regulates the Fate Switch between Cortical and Striatal Interneurons." Neuron 77, no. 1 (January 2013): 83–98. http://dx.doi.org/10.1016/j.neuron.2012.11.035.

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Miquelajauregui, A., T. Van de Putte, A. Polyakov, A. Nityanandam, S. Boppana, E. Seuntjens, A. Karabinos, Y. Higashi, D. Huylebroeck, and V. Tarabykin. "Smad-interacting protein-1 (Zfhx1b) acts upstream of Wnt signaling in the mouse hippocampus and controls its formation." Proceedings of the National Academy of Sciences 104, no. 31 (July 20, 2007): 12919–24. http://dx.doi.org/10.1073/pnas.0609863104.

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Verstappen, G., L. A. van Grunsven, C. Michiels, T. Van de Putte, J. Souopgui, J. Van Damme, E. Bellefroid, J. Vandekerckhove, and D. Huylebroeck. "Atypical Mowat-Wilson patient confirms the importance of the novel association between ZFHX1B/SIP1 and NuRD corepressor complex." Human Molecular Genetics 17, no. 8 (January 4, 2008): 1175–83. http://dx.doi.org/10.1093/hmg/ddn007.

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Gregory-Evans, C. Y., H. Vieira, R. Dalton, G. G. W. Adams, A. Salt, and K. Gregory-Evans. "Ocular coloboma and high myopia with Hirschsprung disease associated with a novel ZFHX1B missense mutation and trisomy 21." American Journal of Medical Genetics 131A, no. 1 (November 15, 2004): 86–90. http://dx.doi.org/10.1002/ajmg.a.30312.

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Garavelli, L., P. Cerruti-Mainardi, R. Virdis, S. Pedori, G. Pastore, M. Godi, S. Provera, et al. "Genitourinary Anomalies in Mowat-Wilson Syndrome with Deletion/Mutation in the Zinc Finger Homeo Box 1B Gene (ZFHX1B)." Hormone Research in Paediatrics 63, no. 4 (2005): 187–92. http://dx.doi.org/10.1159/000085894.

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Sasso, Antun, Ela Paučić-Kirinčić, Silvija Kamber-Makek, Nada Sindičić, S. Brajnović-Zaputović, and Bojana Brajenović-Milić. "Mowat–Wilson syndrome: the clinical report with the novel mutation in ZFHX1B (exon 8: c.2372del C; p.T791fsX816)." Child's Nervous System 24, no. 5 (February 8, 2008): 615–18. http://dx.doi.org/10.1007/s00381-007-0557-5.

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Debruyn, Joke, Eve Seuntjens, and Danny Huylebroeck. "13-P044 Sip1/Zfhx1b is a regulator of Wnt–β-catenin signaling during early midbrain and anterior hindbrain development." Mechanisms of Development 126 (August 2009): S207—S208. http://dx.doi.org/10.1016/j.mod.2009.06.517.

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Goossens, Steven, Viktor Janzen, Sonia Bartunkova, Tomomasa Yokomizo, Benjamin Drogat, Mihaela Crisan, Katharina Haigh, et al. "The EMT regulator Zeb2/Sip1 is essential for murine embryonic hematopoietic stem/progenitor cell differentiation and mobilization." Blood 117, no. 21 (May 26, 2011): 5620–30. http://dx.doi.org/10.1182/blood-2010-08-300236.

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Abstract Zeb2 (Sip1/Zfhx1b) is a member of the zinc-finger E-box–binding (ZEB) family of transcriptional repressors previously demonstrated to regulate epithelial-to-mesenchymal transition (EMT) processes during embryogenesis and tumor progression. We found high Zeb2 mRNA expression levels in HSCs and hematopoietic progenitor cells (HPCs), and examined Zeb2 function in hematopoiesis through a conditional deletion approach using the Tie2-Cre and Vav-iCre recombination mouse lines. Detailed cellular analysis demonstrated that Zeb2 is dispensable for hematopoietic cluster and HSC formation in the aorta-gonadomesonephros region of the embryo, but is essential for normal HSC/HPC differentiation. In addition, Zeb2-deficient HSCs/HPCs fail to properly colonize the fetal liver and/or bone marrow and show enhanced adhesive properties associated with increased β1 integrin and Cxcr4 expression. Moreover, deletion of Zeb2 resulted in embryonic (Tie2-Cre) and perinatal (Vav-icre) lethality due to severe cephalic hemorrhaging and decreased levels of angiopoietin-1 and, subsequently, improper pericyte coverage of the cephalic vasculature. These results reveal essential roles for Zeb2 in embryonic hematopoiesis and are suggestive of a role for Zeb2 in hematopoietic-related pathologies in the adult.

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Dang, Lan TH, and Vincent Tropepe. "FGF dependent regulation of Zfhx1b gene expression promotes the formation of definitive neural stem cells in the mouse anterior neurectoderm." Neural Development 5, no. 1 (2010): 13. http://dx.doi.org/10.1186/1749-8104-5-13.

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Van de Putte, Tom, Annick Francis, Luc Nelles, Leo A. van Grunsven, and Danny Huylebroeck. "Neural crest-specific removal of Zfhx1b in mouse leads to a wide range of neurocristopathies reminiscent of Mowat–Wilson syndrome." Human Molecular Genetics 16, no. 12 (May 3, 2007): 1423–36. http://dx.doi.org/10.1093/hmg/ddm093.

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Choudhuri, Jui, Leah Geiser Roberts, Yan Zhang, Yanhua Wang, and Yanan Fang. "A Rare CD4−CD8+ Adult T-Cell Leukemia/Lymphoma with Unique Molecular Mutations: A Case Report with Literature Review." Case Reports in Hematology 2020 (October 30, 2020): 1–6. http://dx.doi.org/10.1155/2020/8890502.

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Adult T-cell leukemia/lymphoma (ATLL) is a mature T-cell neoplasm caused by infection of the human T-cell lymphotropic virus type 1 (HTLV-1). Most ATLL cases are CD4-positive and CD8-negative. Though rare, there are a few dual negative (CD4−CD8−), dual positive (CD4+CD8+), and CD4−CD8+ cases reported in literature. ATLL is associated with HTLV-1 infection, but HTLV-1 alone cannot cause the malignant transformation of infected T cells. Additional genetic and/or epigenetic events are required for the development of the disease. Here, we report an unusual CD4−CD8+ATLL in a 76-year-old male with a unique molecular genetic profile. Molecular studies revealed alterations in 10 genes. Three of them are predicted to be pathogenic by the computational models, including the frameshift change in ZFHX4 and missense mutations in RHOA and POT1. The specific mutations of POT1 (c.281A > G; p.Q94R), RHOA (c.47G > A; p.C16Y), and ZFHX4 (c.2871delC; p.F958Sfs ∗ 31) have never been previously reported in ATLL to the best of our knowledge. The clinical significance of other genetic alterations is unknown. Further research is warranted to correlate this patient’s molecular findings with other ATLL cases. Correlation specifically with other cases of CD8+ ATLL could prove to be useful in understanding the pathogenesis of this rare variant of an already rare form of leukemia/lymphoma.

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Yang, Seung-Ae. "Association study between ZFHX3 gene polymorphisms and obesity in Korean population." Journal of Exercise Rehabilitation 13, no. 4 (August 29, 2017): 491–94. http://dx.doi.org/10.12965/jer.1735080.540.

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Balzani, Edoardo, Glenda Lassi, Silvia Maggi, Siddharth Sethi, Michael J. Parsons, Michelle Simon, Patrick M. Nolan, and Valter Tucci. "The Zfhx3-Mediated Axis Regulates Sleep and Interval Timing in Mice." Cell Reports 16, no. 3 (July 2016): 615–21. http://dx.doi.org/10.1016/j.celrep.2016.06.017.

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