Oct4 plays a role in 2, 3, 7, 8 - tetrachlorobenzo-p-dioxin (TCDD) inducing cleft palate and inhibiting mesenchymal proliferation.

[1]  Yan Zhang,et al.  2,3,7,8-Tetrachlorodibenzo-p-dioxin Promotes Proliferation of Astrocyte Cells via the Akt/STAT3/Cyclin D1 Pathway. , 2019, Biomedical and environmental sciences : BES.

[2]  A. Hirata,et al.  Cleft palate formation after palatal fusion occurs due to the rupture of epithelial basement membranes. , 2018, Journal of cranio-maxillo-facial surgery : official publication of the European Association for Cranio-Maxillo-Facial Surgery.

[3]  P. Chou,et al.  Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin increases the activation of aryl hydrocarbon receptor and is associated with the aggressiveness of osteosarcoma MG-63 osteoblast-like cells , 2018, Oncology letters.

[4]  Yue Liu,et al.  OCT4B regulates p53 and p16 pathway genes to prevent apoptosis of breast cancer cells. , 2018, Oncology letters.

[5]  Wei Zhang,et al.  Alterations in DNA methyltransferases and methyl-CpG binding domain proteins during cleft palate formation as induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in mice. , 2018, Molecular medicine reports.

[6]  K. Tsim,et al.  2,3,7,8-Tetrachlorodibenzo-p-dioxin induces alterations in myogenic differentiation of C2C12 cells. , 2018, Environmental pollution.

[7]  Ding-wen Zhang,et al.  Preliminary research on DNA methylation changes during murine palatogenesis induced by TCDD. , 2017, Journal of cranio-maxillo-facial surgery : official publication of the European Association for Cranio-Maxillo-Facial Surgery.

[8]  Lanjuan Li,et al.  Tryptophan derivatives regulate the transcription of Oct4 in stem-like cancer cells , 2015, Nature Communications.

[9]  Byeong-chun Lee,et al.  Oct4 overexpression facilitates proliferation of porcine fibroblasts and development of cloned embryos , 2014, Zygote.

[10]  H. Schöler,et al.  Role of Oct4 in the early embryo development , 2014, Cell Regeneration.

[11]  Yixuan Fan,et al.  Oct4 and Sox2 overexpression improves the proliferation and differentiation of bone mesenchymal stem cells in Xiaomeishan porcine. , 2013, Genetics and molecular research : GMR.

[12]  T. Babak,et al.  Oct4 Is Required ∼E7.5 for Proliferation in the Primitive Streak , 2013, PLoS genetics.

[13]  M. Medvedovic,et al.  Disruption of Aryl Hydrocarbon Receptor Homeostatic Levels during Embryonic Stem Cell Differentiation Alters Expression of Homeobox Transcription Factors that Control Cardiomyogenesis , 2013, Environmental health perspectives.

[14]  N. Takahashi,et al.  Teratogenic Factors Affect Transcription Factor Expression , 2013, Bioscience, biotechnology, and biochemistry.

[15]  R. Redett,et al.  Cleft Lip and Palate , 2013, Eplasty.

[16]  Lei Chen,et al.  OCT4 Positively Regulates Survivin Expression to Promote Cancer Cell Proliferation and Leads to Poor Prognosis in Esophageal Squamous Cell Carcinoma , 2012, PloS one.

[17]  Xiaomeng He,et al.  2,3,7,8-Tetrachlorodibenzo-p-dioxin induces a proteomic pattern that defines cleft palate formation in mice. , 2012, Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association.

[18]  T. Beaty,et al.  BMP4 Was Associated with NSCL/P in an Asian Population , 2012, PloS one.

[19]  Natalia B. Ivanova,et al.  Distinct lineage specification roles for NANOG, OCT4, and SOX2 in human embryonic stem cells. , 2012, Cell stem cell.

[20]  R. Jiang,et al.  Palatogenesis: morphogenetic and molecular mechanisms of secondary palate development , 2012, Development.

[21]  H. Schöler,et al.  Concise Review: Oct4 and More: The Reprogramming Expressway , 2012, Stem cells.

[22]  J. Santos,et al.  Risk variants in BMP4 promoters for nonsyndromic cleft lip/palate in a Chilean population , 2011, BMC Medical Genetics.

[23]  J. Trosko,et al.  Metformin Represses Self-Renewal of the Human Breast Carcinoma Stem Cells via Inhibition of Estrogen Receptor-Mediated OCT4 Expression , 2011, PloS one.

[24]  Holger Schwender,et al.  Evidence for gene‐environment interaction in a genome wide study of nonsyndromic cleft palate , 2011, Genetic epidemiology.

[25]  A. Yen,et al.  Activation of the aryl hydrocarbon receptor AhR Promotes retinoic acid-induced differentiation of myeloblastic leukemia cells by restricting expression of the stem cell transcription factor Oct4. , 2011, Cancer research.

[26]  M. Pisano,et al.  Palate morphogenesis: current understanding and future directions. , 2010, Birth defects research. Part C, Embryo today : reviews.

[27]  Jungho Kim,et al.  Oct-4 controls cell-cycle progression of embryonic stem cells , 2009, The Biochemical journal.

[28]  J. Little,et al.  Cleft lip and palate , 2009, The Lancet.

[29]  Lin Qiu,et al.  Transforming growth factor-β3 expression up-regulates on cleft palates induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in mice , 2009, Toxicology and industrial health.

[30]  A. Jugessur,et al.  Mutations in BMP4 are associated with subepithelial, microform, and overt cleft lip. , 2009, American journal of human genetics.

[31]  A. Nawshad Palatal seam disintegration: To die or not to die? that is no longer the question , 2008, Developmental dynamics : an official publication of the American Association of Anatomists.

[32]  K. Mishima,et al.  Morphological and immunohistochemical studies on cleft palates induced by 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin in mice , 2008, Congenital anomalies.

[33]  C. Tohyama,et al.  The 2005 World Health Organization reevaluation of human and Mammalian toxic equivalency factors for dioxins and dioxin-like compounds. , 2006, Toxicological sciences : an official journal of the Society of Toxicology.

[34]  K. Mishima,et al.  Cleft lip and palate in mice treated with 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin: a morphological in vivo study , 2006, Congenital anomalies.

[35]  Emily A. Stevens,et al.  The Teratogenic Sensitivity to 2,3,7,8-Tetrachlorodibenzo-p-dioxin Is Modified by a Locus on Mouse Chromosome 3 , 2006, Molecular Pharmacology.

[36]  M. Marazita,et al.  Current concepts in the embryology and genetics of cleft lip and cleft palate. , 2004, Clinics in plastic surgery.

[37]  D. Waxman,et al.  P450 gene induction by structurally diverse xenochemicals: central role of nuclear receptors CAR, PXR, and PPAR. , 1999, Archives of biochemistry and biophysics.

[38]  R. Baggs,et al.  Aryl hydrocarbon receptor activation in genital tubercle, palate, and other embryonic tissues in 2,3,7, 8-tetrachlorodibenzo-p-dioxin-responsive lacZ mice. , 1998, Toxicology and applied pharmacology.

[39]  Y. Bergman,et al.  Retinoic acid represses Oct-3/4 gene expression through several retinoic acid-responsive elements located in the promoter-enhancer region , 1994, Molecular and cellular biology.

[40]  L S Birnbaum,et al.  A critical review of the developmental toxicity and teratogenicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin: recent advances toward understanding the mechanism. , 1990, Teratology.

[41]  K. Yamashita,et al.  Pathogenesis of cleft palate in mouse embryos exposed to 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD). , 2000, Teratogenesis, carcinogenesis, and mutagenesis.