S
Stefan A. Haas
Researcher at Max Planck Society
Publications - 88
Citations - 13764
Stefan A. Haas is an academic researcher from Max Planck Society. The author has contributed to research in topics: Gene & X-linked intellectual disability. The author has an hindex of 47, co-authored 86 publications receiving 11715 citations. Previous affiliations of Stefan A. Haas include German Cancer Research Center.
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Journal ArticleDOI
Primer design for large scale sequencing
TL;DR: PRIDE, a primer design program that automatically designs primers in single contigs or whole sequencing projects to extend the already known sequence and to double strand single-stranded regions, is developed.
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Next-Generation Sequencing Identifies Mutations of SMPX, which Encodes the Small Muscle Protein, X-Linked, as a Cause of Progressive Hearing Impairment
Margit Schraders,Stefan A. Haas,N.J.D. Weegerink,Jaap Oostrik,Hao Hu,Lies H. Hoefsloot,Sriram Kannan,Patrick L. M. Huygen,Ronald J.E. Pennings,Ronald J.C. Admiraal,Vera M. Kalscheuer,Henricus P. M. Kunst,Hannie Kremer +12 more
TL;DR: It is hypothesize that SMPX functions in inner ear development and/or maintenance in the IGF-1 pathway, the integrin pathway through Rac1, or both, and that the mutations cosegregated with hearing impairment.
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Genome wide identification and classification of alternative splicing based on EST data
TL;DR: High quality exon-intron boundaries are used to predict constitutive and alternative splicing ranked by confidence values, aiming to facilitate large-scale analysis of alternativesplicing and splicing in general.
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Comparing active and repressed expression states of genes controlled by the Polycomb/Trithorax group proteins
Christian Beisel,Andreas Buness,Ian M. Roustan-Espinosa,B. Koch,Sabine Schmitt,Stefan A. Haas,Marc Hild,Tomonori Katsuyama,Renato Paro +8 more
TL;DR: Besides its presumptive function in recruiting PcG complexes to their site of action, the results now uncover that Pho plays an additional role in the repression of already induced genes.
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Involvement of the kinesin family members KIF4A and KIF5C in intellectual disability and synaptic function
Marjolein H. Willemsen,Wei Ba,Willemijn M. Wissink-Lindhout,Arjan P.M. de Brouwer,Stefan A. Haas,M Bienek,Hao Hu,Lisenka E.L.M. Vissers,Hans van Bokhoven,Vera M. Kalscheuer,Nael Nadif Kasri,Tjitske Kleefstra +11 more
TL;DR: The results suggest that mutations in KIF4A and KIF5C cause ID by tipping the balance between excitatory and inhibitory synaptic excitability.