Titlebook: Genomic Disorders; The Genomic Basis of James R. Lupski,Pawel Stankiewicz Book 2006 Humana Press 2006 DNA.chromosome.diseases.evolution.gen

Jackson

書目名稱Genomic Disorders影響因子(影響力)




書目名稱Genomic Disorders影響因子(影響力)學科排名




書目名稱Genomic Disorders網(wǎng)絡(luò)公開度




書目名稱Genomic Disorders網(wǎng)絡(luò)公開度學科排名




書目名稱Genomic Disorders被引頻次




書目名稱Genomic Disorders被引頻次學科排名




書目名稱Genomic Disorders年度引用




書目名稱Genomic Disorders年度引用學科排名




書目名稱Genomic Disorders讀者反饋




書目名稱Genomic Disorders讀者反饋學科排名

–FER

Francis Balestra,Gérard Ghibaudosignificant role not only in common recurrent deletions and duplications, but also in other rearrangements including unusual sized (i.e., uncommon, recurrent and nonrecurrent) chromosomal deletions, reciprocal translocations, and marker chromosomes. DNA sequence analysis from both common and unusual

首創(chuàng)精神

暴行

Devices for Cardiac Resynchronization:e to the choice of discrete sites for strand exchange have been identified. NF1 -REP-mediated NF1 microdeletions involve 13 additional genes, whereas JJAZ1 -mediated microdeletions involve the same genes but one. NF1 microdeletions are of great interest because they predispose to a heavy tumor burde

Intend

沒血色

Smith-Magenis Syndrome Deletion, Reciprocal Duplication dup(17)(p11.2p11.2), and Other Proximal 17p significant role not only in common recurrent deletions and duplications, but also in other rearrangements including unusual sized (i.e., uncommon, recurrent and nonrecurrent) chromosomal deletions, reciprocal translocations, and marker chromosomes. DNA sequence analysis from both common and unusual

沒血色

Chromosome 22q11.2 Rearrangement Disorders q11.2) syndrome. In contrast to VCFS/DGS, dup(22)(q11.2; q11.2) and CES, der(22) syndrome is caused by a different molecular mechanism. Der(22) disorder arises in offspring of normal carriers of the constitutional t(1 1 ;22) (q23.3; q1 1.2) translocation by recombination between AT-rich (high AT se

混合,攙雜

Neurofibromatosis 1e to the choice of discrete sites for strand exchange have been identified. NF1 -REP-mediated NF1 microdeletions involve 13 additional genes, whereas JJAZ1 -mediated microdeletions involve the same genes but one. NF1 microdeletions are of great interest because they predispose to a heavy tumor burde

dragon

structural features, architecture, and evolution of the human genome. The authors demonstrate how such architectural features may be important to both evolution and to explaining the susceptibility to those DNA rearrangements associated with disease. Technologies to assay for such structural variat

euphoria

https://doi.org/10.1007/978-3-658-19630-1omic tools, the understanding of this highly sophisticated sensory neuronal pathway has been rather sketchy. In this chapter we summarize the relevant progress made in the last decade, and highlight the initial elucidation of two classes of olfactory deficits and their possible underlying genetic mechanisms.