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Annie Yang

Researcher at Harvard University

Publications -  34
Citations -  19781

Annie Yang is an academic researcher from Harvard University. The author has contributed to research in topics: Gene & Transactivation. The author has an hindex of 30, co-authored 34 publications receiving 19024 citations. Previous affiliations of Annie Yang include Genentech.

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Identification and analysis of functional elements in 1% of the human genome by the ENCODE pilot project

Ewan Birney, +320 more
- 14 Jun 2007 - 
TL;DR: Functional data from multiple, diverse experiments performed on a targeted 1% of the human genome as part of the pilot phase of the ENCODE Project are reported, providing convincing evidence that the genome is pervasively transcribed, such that the majority of its bases can be found in primary transcripts.
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p63 is essential for regenerative proliferation in limb, craniofacial and epithelial development

TL;DR: It is reported that mice homozygous for a disrupted p63 gene have major defects in their limb, craniofacial and epithelial development, and results indicate that p63 is critical for maintaining the progenitor-cell populations that are necessary to sustain epithelialDevelopment and morphogenesis.
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p63, a p53 homolog at 3q27-29, encodes multiple products with transactivating, death-inducing, and dominant-negative activities.

TL;DR: The cloning of p63, a gene at chromosome 3q27-29 that bears strong homology to the tumor suppressor p53 and to the related gene, p73, is described and the possibility of physiological interactions among members of the p53 family is suggested.
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Monoallelically expressed gene related to p53 at 1p36, a region frequently deleted in neuroblastoma and other human cancers.

TL;DR: The demonstration that p73 is monoallelically expressed supports the notion that it is a candidate gene in neuroblastoma and proposes that the disregulation of p73 contributes to tumorigenesis and that p53-related proteins operate in a network of developmental and cell cycle controls.
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p73-deficient mice have neurological, pheromonal and inflammatory defects but lack spontaneous tumours

TL;DR: It is shown that mice functionally deficient for all p73 isoforms exhibit profound defects, including hippocampal dysgenesis, hydrocephalus, chronic infections and inflammation, as well as abnormalities in pheromone sensory pathways, and there is a marked divergence in the physiological functions of the p53 family members.