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Amos J. Simon
Researcher at Sheba Medical Center
Publications - 111
Citations - 4141
Amos J. Simon is an academic researcher from Sheba Medical Center. The author has contributed to research in topics: Immunodeficiency & Severe combined immunodeficiency. The author has an hindex of 32, co-authored 99 publications receiving 3574 citations. Previous affiliations of Amos J. Simon include Tel Aviv University & Boston Children's Hospital.
Papers
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Journal ArticleDOI
Nuclear membrane protein LAP2β mediates transcriptional repression alone and together with its binding partner GCL (germ-cell-less)
Einav Nili,Gady S. Cojocaru,Yael Kalma,Doron Ginsberg,Neal G. Copeland,Debra J. Gilbert,Nancy A. Jenkins,Raanan Berger,Sigal Shaklai,Ninette Amariglio,Frida Brok-Simoni,Amos J. Simon,Gideon Rechavi +12 more
TL;DR: It is demonstrated here that LAP2beta is also capable of reducing the transcriptional activity of the E2F-DP complex and that it is more potent than mGCL in doing so.
Journal ArticleDOI
The nuclear-envelope protein and transcriptional repressor LAP2β interacts with HDAC3 at the nuclear periphery, and induces histone H4 deacetylation
Raz Somech,Raz Somech,Raz Somech,Sigal Shaklai,Sigal Shaklai,Orit Geller,Orit Geller,Ninette Amariglio,Ninette Amariglio,Amos J. Simon,Amos J. Simon,Gideon Rechavi,Gideon Rechavi,Einav Nili Gal-Yam,Einav Nili Gal-Yam +14 more
TL;DR: It is shown that LAP2β interacts at the nuclear envelope with HDAC3, a class-I histone deacetylase, and that TSA (an HDAC inhibitor) abrogates LAP1β's repressive activity and that Lap2β is capable of inducing histone-H4 deacetolation.
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Effect of CD3δ Deficiency on Maturation of α/β and γ/δ T-Cell Lineages in Severe Combined Immunodeficiency
TL;DR: Three closely related infants with a form of severe combined immunodeficiency characterized by the absence of T cells but normal numbers of B cells were found to have an identical germ-line mutation in the CD3δ gene.
Journal ArticleDOI
The CC2D1A , a member of a new gene family with C2 domains, is involved in autosomal recessive non-syndromic mental retardation
Lina Basel-Vanagaite,Revital Attia,Michal Yahav,Russell J. Ferland,Limor Anteki,Christopher A. Walsh,Tsviya Olender,Rachel Straussberg,Nurit Magal,Ellen Taub,Valerie Drasinover,Anna Alkelai,Dani Bercovich,Gideon Rechavi,Amos J. Simon,Mordechai Shohat +15 more
TL;DR: A previously unknown signal transduction pathway is important in human cognitive development and a protein truncating mutation was identified in the gene CC2D1A in nine consanguineous families with severe autosomal recessive NSMR.
Journal ArticleDOI
A LAD-III syndrome is associated with defective expression of the Rap-1 activator CalDAG-GEFI in lymphocytes, neutrophils, and platelets
Ronit Pasvolsky,Sara W. Feigelson,Sara Sebnem Kilic,Amos J. Simon,Guy Tal-Lapidot,Valentin Grabovsky,Jill R. Crittenden,Ninette Amariglio,Michal Safran,Ann M. Graybiel,Gideon Rechavi,Shifra Ben-Dor,Amos Etzioni,Amos Etzioni,Ronen Alon +14 more
TL;DR: Two new LAD cases are reported in which lymphocytes, neutrophils, and platelets share severe defects in β1, β2, and β3 integrin activation, and CalDAG-GEFI is identified as a critical regulator of inside-out integrinactivation in human T lymphocytes.