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Cell|September 6, 1991
napts, a mutation affecting sodium channel activity in Drosophila, is an allele of mle, a regulator of X chromosome transcriptionM J Kernan, M I Kuroda, R Kreber, et al.Science (New York, N.Y.)|November 26, 2002
Extent of chromatin spreading determined by roX RNA recruitment of MSL proteinsYongkyu Park, Richard L Kelley, Hyangyee Oh, et al.Nature Structural & Molecular Biology|August 4, 2009
Drosophila MSL complex globally acetylates H4K16 on the male X chromosome for dosage compensationMarnie E Gelbart, Erica Larschan, Shouyong Peng, et al.Gan to Kagaku Ryoho. Cancer & Chemotherapy|May 2, 2001
[Metastatic liver tumor arising from prostate cancer following transurethral resection of the prostate--a report of two cases]N Yamamoto, X Zhang, S Soramoto, et al.Genes & Development|October 3, 2009
Long-range spreading of dosage compensation in Drosophila captures transcribed autosomal genes inserted on XAndrey A Gorchakov, Artyom A Alekseyenko, Peter Kharchenko, et al.Cell|February 21, 1997
roX1 RNA paints the X chromosome of male Drosophila and is regulated by the dosage compensation systemV H Meller, K H Wu, G Roman, et al.Genes & Development|March 21, 2006
High-resolution ChIP-chip analysis reveals that the Drosophila MSL complex selectively identifies active genes on the male X chromosomeArtyom A Alekseyenko, Erica Larschan, Weil R Lai, et al.Cold Spring Harbor Symposia on Quantitative Biology|March 27, 2007
MSL complex associates with clusters of actively transcribed genes along the Drosophila male X chromosomeE Larschan, A A Alekseyenko, W R Lai, et al.Chromosome Research : an International Journal on the Molecular, Supramolecular and Evolutionary Aspects of Chromosome Biology|September 1, 1994
Histone H4 acetylated at lysine 16 and proteins of the Drosophila dosage compensation pathway co-localize on the male X chromosome through mitosisJ S Lavender, A J Birley, M J Palmer, et al.Acta Neurochirurgica|June 23, 2007
Multiple peripheral middle cerebral artery aneurysms associated with Behcet's diseaseY Kaku, J-I Hamada, J-I Kuroda, et al.Pageof 12