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      Transforming growth factor-beta 3 is required for secondary palate fusion.

      Nature genetics

      physiology, analysis, Transforming Growth Factor beta, Transcription Factors, Repressor Proteins, embryology, chemistry, Palate, Morphogenesis, Molecular Sequence Data, Mice, Knockout, Mice, Inbred C57BL, Mice, Mesoderm, Homeodomain Proteins, Goosecoid Protein, Extracellular Matrix Proteins, DNA-Binding Proteins, Cytoskeletal Proteins, genetics, Cleft Palate, Base Sequence, Animals

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          Abstract

          Mice lacking TGF-beta 3 exhibit an incompletely penetrant failure of the palatal shelves to fuse leading to cleft palate. The defect appears to result from impaired adhesion of the apposing medial edge epithelia of the palatal shelves and subsequent elimination of the mid-line epithelial seam. No craniofacial abnormalities were observed. This result demonstrates that TGF-beta 3 affects palatal shelf fusion by an intrinsic, primary mechanism rather than by effects secondary to craniofacial defects.

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          Most cited references 34

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          Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction.

          A new method of total RNA isolation by a single extraction with an acid guanidinium thiocyanate-phenol-chloroform mixture is described. The method provides a pure preparation of undegraded RNA in high yield and can be completed within 4 h. It is particularly useful for processing large numbers of samples and for isolation of RNA from minute quantities of cells or tissue samples.
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            Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease.

            Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-beta 1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-beta 1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-beta 1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.
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              • Record: found
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              Simplified mammalian DNA isolation procedure.

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                Author and article information

                Journal
                10.1038/ng1295-409
                3855390
                7493021

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