The zinc finger transcription factor 191 is required for early embryonic development and cell proliferation

Li, Jianzhong; Chen, Xia; Yang, Hua; Wang, Shuiliang; Guo, Binhui; Yu, Lingjia; Wang, Zhugang; Fu, Jian

doi:10.1016/j.yexcr.2006.08.020

Cited by 29 publications

(39 citation statements)

References 41 publications

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“…Nevertheless, abnormalities other than the CNS myelination defect were not observed in our Zfp191 mutants. Interestingly, a previously published study described the generation of a Zfp191 null mouse mutant that displayed an embryoniclethal phenotype at E7.5 (Li et al 2006). This differs Genes with greater than twofold reduction in expression in the mutants are shown here.…”

Section: Discussionmentioning

confidence: 99%

“…Although the reason for this difference is unclear, one possible explanation emanates from the observation that the two null alleles are not identical. In the Zfp191 null mutants described here, the PGK-neo cassette used for positive selection of embryonic stem (ES) cells has been removed, whereas it remains in the Zfp191-null allele described by Li et al (2006). Previous studies have shown that the presence of this selection cassette can modify the activity of genes in the vicinity of the targeted allele (Pham et al 1996;Xin et al 2005).…”

Section: Zfp191 Is Required For Cns Myelination Genes and Development 307mentioning

confidence: 99%

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ZFP191 is required by oligodendrocytes for CNS myelination

et al. 2010

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The controlling factors that prompt mature oligodendrocytes to myelinate axons are largely undetermined. In this study, we used a forward genetics approach to identify a mutant mouse strain characterized by the absence of CNS myelin despite the presence of abundant numbers of late-stage, process-extending oligodendrocytes. Through linkage mapping and complementation testing, we identified the mutation as a single nucleotide insertion in the gene encoding zinc finger protein 191 (Zfp191), which is a widely expressed, nuclear-localized protein that belongs to a family whose members contain both DNA-binding zinc finger domains and protein-proteininteracting SCAN domains. Zfp191 mutants express an array of myelin-related genes at significantly reduced levels, and our in vitro and in vivo data indicate that mutant ZFP191 acts in a cell-autonomous fashion to disrupt oligodendrocyte function. Therefore, this study demonstrates that ZFP191 is required for the myelinating function of differentiated oligodendrocytes.[Keywords: Mouse mutant; forward genetics; hypomyelination; conditional allele; zinc finger protein; scan domain] Supplemental material is available at http://www.genesdev.org.

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Section: Discussionmentioning

confidence: 99%

Section: Zfp191 Is Required For Cns Myelination Genes and Development 307mentioning

confidence: 99%

ZFP191 is required by oligodendrocytes for CNS myelination

et al. 2010

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“…ZNF191 has been identified in a T cell line, contains four C 2 H 2 zinc finger domains, and znf191-deficient mice died at ϳ7.5 days after fertilization (64). ZNF397 possesses nine C 2 H 2 zinc finger domains and is expressed in the spleen and thymus at low levels and acts as a transcriptional activator (63).…”

Section: Discussionmentioning

confidence: 99%

Enhanced Th2 Cell Differentiation and Allergen-Induced Airway Inflammation in Zfp35-Deficient Mice

Kitajima

Iwamura

Miki-Hosokawa

et al. 2009

The Journal of Immunology

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Studies of human asthma and of animal models of allergic airway inflammation revealed a crucial role for Th2 cells in the pathogenesis of allergic asthma. Kruppel-type zinc finger proteins are the largest family of a regulatory transcription factor for cellular development and function. Zinc finger protein (Zfp) 35 is an 18-zinc finger motif-containing Kruppel-type zinc finger protein, while its function remains largely unknown. The aim of this study was to clarify the role of Zfp35 in the pathogenesis of Th2-dependent allergic inflammation, such as allergic asthma. We examined airway eosinophilic inflammation and hyperresponsiveness in two mouse models, which use our newly generated Zfp35-deficient (Zfp35−/−) mice and adoptive transfer of cells. In Zfp35−/− mice, Th2 cell differentiation, Th2 cytokine production, eosinophilic inflammation, and airway hyperresponsiveness were substantially enhanced. Furthermore, adoptive transfer of Ag-sensitized Zfp35−/− CD4 T cells into the asthmatic mice resulted in enhanced airway inflammation and airway hyperresponsiveness. These results indicate that Zfp35 controls Th2 cell differentiation, allergic airway inflammation, and airway hyperresponsiveness in a negative manner. Thus, Zfp35 may control Th2-dependent diseases, such as allergic asthma.

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“…-/-mouse demonstrated that this protein is indispensable for early embryonic development; Zfp191 -/-mice died before embryonic day 7.5 (Li et al, 2006). ZNF24 was first noticed for its capacity to bind to a tandem repeat TCAT sequence in the first intron of human tyrosine hydroxylase (TH) and to negatively regulate its transcription (Albanese et al, 2001).…”

Section: Examination Of the Zfp191mentioning

confidence: 99%

“…+/-mice were provided by Prof. Jiliang Fu (Li et al, 2006). Zfp191 +/-were backcrossed more than 10 times to the C57BL/6J genetic background.…”

Section: Zfp191mentioning

confidence: 99%

Resistance to lipopolysaccharide-induced endotoxic shock in heterozygous Zfp191 gene-knockout mice

Sun¹,

Wang²,

Yang³

et al. 2011

Genet. Mol. Res.

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ABSTRACT. Zinc finger protein 191, ZNF24 and Zfp191 in both humans and mice belong to the SCAN domain subfamily of Krüppel-like zinc finger transcription factors. Previous studies have suggested that Zfp191 is a pleiotropic factor involved in embryonic development, hematopoiesis and tumorigenesis. However, little is known about its target genes or its role in other physiological and pathological processes. We have identified the putative target genes of Zfp191, using an in silico genome-wide scan. Three hundred and fifty-five putative target genes were identified, which were enriched into the pathways of immune response according to the pathway analysis. These targets indicated that Zfp191 may function as a mediator of the immune response. This was verified in mice heterozygous for Zfp191 (Zfp191 +/-) using a lipopolysaccharide (LPS)-induced endotoxic shock model. After LPS injection, Zfp191 +/-mice produced significantly less IL-1β and IL-6 compared to wild-type mice and were resistant to LPS-induced endotoxic ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 10 (4): 1712-3721 (2011) Resistance to endotoxic shock in Zfp191 gene-knockout mice 3713shock. The loss of Zfp191 may suppress systemic inflammation by reducing these cytokine levels during LPS-induced endotoxic shock.

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The zinc finger transcription factor 191 is required for early embryonic development and cell proliferation

Cited by 29 publications

References 41 publications

ZFP191 is required by oligodendrocytes for CNS myelination

ZFP191 is required by oligodendrocytes for CNS myelination

Enhanced Th2 Cell Differentiation and Allergen-Induced Airway Inflammation in Zfp35-Deficient Mice

Resistance to lipopolysaccharide-induced endotoxic shock in heterozygous Zfp191 gene-knockout mice

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