id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
work_wx7cgwo7ifd2jbnialwd5iulam	Romeo Carrozzo	Inter- and Intrachromosomal Rearrangements Are Both Involved in the Origin of 15q11-q13 Deletions in Prader-Willi Syndrome	1997.0	4	.pdf	application/pdf	2936	227	60	In addideletion spans a region of Ç4 Mb and invariably intion, marker ATC3C11, mapping õ1 Mb from the disvolves the paternally derived homologue (Robinson et tal deletion breakpoint (S. tions in PWS, we genotyped 10 three-generation families D15S165 in male meiosis is taken into account, the idenof PWS-deletion patients, using microsatellite markers tification, in five of seven cases, of a different grandparenflanking the common deletion region. duplication event may arise from the unequal recombiPWS families the data were consistent with an intrachromosomal mechanism being responsible for the deletion.nation between repetitive elements interspersed MR, Nakao M, Surti U, et al (1995) Molecular characteriza-the formation of an intrachromosomal loop, either durtion of two proximal deletion breakpoint regions in bothing meiosis or as a somatic event, followed by an exciPrader-Willi and Angelman syndrome patients. grandparental markers flanking the deleted region in Dutly F, Schinzel A (1996) Unequal interchromosomal rearrangements may result in elastin gene deletions causing the15 patients and their parents demonstrated a recomWilliams-Beuren syndrome.	./cache/work_wx7cgwo7ifd2jbnialwd5iulam.pdf	./txt/work_wx7cgwo7ifd2jbnialwd5iulam.txt