Somatic mutations and progressive monosomy modify SAMD9-related phenotypes in humans-Reference-Cited by-同舟云学术

Somatic mutations and progressive monosomy modify SAMD9-related phenotypes in humans

Published:2017-03-27 Issue:5 Volume:127 Page:1700-1713
ISSN:0021-9738
Container-title:Journal of Clinical Investigation
language:en
Short-container-title:

Author:

Buonocore Federica,Kühnen Peter,Suntharalingham Jenifer P.,Del Valle Ignacio,Digweed Martin,Stachelscheid Harald^ORCID,Khajavi Noushafarin,Didi Mohammed,Brady Angela F.,Blankenstein Oliver^ORCID,Procter Annie M.,Dimitri Paul,Wales Jerry K.H.,Ghirri Paolo,Knöbl Dieter,Strahm Brigitte,Erlacher Miriam,Wlodarski Marcin W.,Chen Wei,Kokai George K.,Anderson Glenn,Morrogh Deborah,Moulding Dale A.,McKee Shane A.,Niemeyer Charlotte M.,Grüters Annette,Achermann John C.

Publisher

American Society for Clinical Investigation

Subject

General Medicine

Link

https://www.jci.org/articles/view/91913/files/pdf

Reference33 articles.

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2. Mouse Samd9l is not a functional paralogue of the human SAMD9, the gene mutated in normophosphataemic familial tumoral calcinosis

3. The Samd9L Gene: Transcriptional Regulation and Tissue-Specific Expression in Mouse Development

4. Overexpression of SAMD9 suppresses tumorigenesis and progression during non small cell lung cancer

5. Human sterile alpha motif domain 9, a novel gene identified as down-regulated in aggressive fibromatosis, is absent in the mouse;Li;BMC Genomics,2007

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