Találati lista | Tudóstér

001-es BibID:	BIBFORM035749
Első szerző:	Chan, Betty
Cím:	SAP couples Fyn to SLAM immune receptors / Chan Betty, Lanyi Arpad, Song Hyun Kyu, Griesbach Jan, Simarro-Grande Maria, Poy Florence, Howie Duncan, Sumegi Janos, Terhorst Cox, Eck Michael J.
Dátum:	2003
ISSN:	1465-7392
Megjegyzések:	SAP (SLAM-associated protein) is a small lymphocyte-specific signalling molecule that is defective or absent in patients with X-linked lymphoproliferative syndrome (XLP). Consistent with its single src homology 2 (SH2) domain architecture and unusually high affinity for SLAM (also called CD150), SAP has been suggested to function by blocking binding of SHP-2 or other SH2-containing signalling proteins to SLAM receptors. Additionally, SAP has recently been shown to be required for recruitment and activation of the Src-family kinase FynT after SLAM ligation. This signalling 'adaptor' function has been difficult to conceptualize, because unlike typical SH2-adaptor proteins, SAP contains only a single SH2 domain and lacks other recognized protein interaction domains or motifs. Here, we show that the SAP SH2 domain binds to the SH3 domain of FynT and directly couples FynT to SLAM. The crystal structure of a ternary SLAM-SAP-Fyn-SH3 complex reveals that SAP binds the FynT SH3 domain through a surface-surface interaction that does not involve canonical SH3 or SH2 binding interactions. The observed mode of binding to the Fyn-SH3 domain is expected to preclude the auto-inhibited conformation of Fyn, thereby promoting activation of the kinase after recruitment. These findings broaden our understanding of the functional repertoire of SH3 and SH2 domains.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Nature Cell Biology. - 5 : 2 (2003), p. 155-160. -
További szerzők:	Lányi Árpád (1962-) (biológus, immunológus) Song, Hyun Kyu Griesbach, Jan Simarro-Grande, Maria Poy, Florence Howie, Duncan Sümegi János Terhorst, Cox Eck, Michael J.
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM096176
035-os BibID:	(WoS)000660626300005 (Scopus)85107510241
Első szerző:	Fuxreiter Mónika (kutató vegyész)
Cím:	Generic nature of the condensed states of proteins / Monika Fuxreiter, Michele Vendruscolo
Dátum:	2021
ISSN:	1465-7392
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Nature Cell Biology. - 23 : 6 (2021), p. 587-594. -
További szerzők:	Vendruscolo, Michele
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM019005
Első szerző:	Iacovino, Michelina
Cím:	HoxA3 is an apical regulator of haemogenic endothelium / Iacovino Michelina, Chong Diana, Szatmari Istvan, Hartweck Lynn, Rux Danielle, Caprioli Arianna, Cleaver Ondine, Kyba Michael
Dátum:	2011
ISSN:	1465-7392
Megjegyzések:	During development, haemogenesis occurs invariably at sites of vasculogenesis. Between embryonic day (E) 9.5 and E10.5 in mice, endothelial cells in the caudal part of the dorsal aorta generate haematopoietic stem cells and are referred to as haemogenic endothelium. The mechanisms by which haematopoiesis is restricted to this domain, and how the morphological transformation from endothelial to haematopoietic is controlled are unknown. We show here that HoxA3, a gene uniquely expressed in the embryonic but not yolk sac vasculature, restrains haematopoietic differentiation of the earliest endothelial progenitors, and induces reversion of the earliest haematopoietic progenitors into CD41-negative endothelial cells. This reversible modulation of endothelial-haematopoietic state is accomplished by targeting key haematopoietic transcription factors for downregulation, including Runx1, Gata1, Gfi1B, Ikaros, and PU.1. Through loss-of-function, and gain-of-function epistasis experiments, and the identification of antipodally regulated targets, we show that among these factors, Runx1 is uniquely able to erase the endothelial program set up by HoxA3. These results suggest both why a frank endothelium does not precede haematopoiesis in the yolk sac, and why haematopoietic stem cell generation requires Runx1 expression only in endothelial cells.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok levél
Megjelenés:	Nature Cell Biology. - 13 : 1 (2011), p. 72-78. -
További szerzők:	Chong, Diana Szatmári István (1971-) (biológus) Hartweck, Lynn Rux, Danielle Caprioli, Arianna Cleaver, Ondine Kyba, Michael
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	bibEBI12985
Első szerző:	Wikonkál Norbert, M.
Cím:	Inactivating E2f1 reverts apoptosis resistance and cancer sensitivity in Trp53-deficient mice / Wikonkal, N. M., Remenyik, É., Knezevich, D., Zhang, W., Liu, M., Zhao, H., Berton, T. R., Johnson, D. G., Brash, D. E.
Dátum:	2003
Megjegyzések:	The E2f1 transcription factor, which regulates genes required for S-phase entry, also induces apoptosis by transcriptional and post-translational mechanisms. As E2f1 is inducible by DNA damage we investigated its importance in vivo in ultraviolet (UV)-induced apoptosis, a protective mechanism that prevents the epidermis from accumulating UV-induced mutations. Contrary to expectation, E2f1-/- mice demonstrated enhanced keratinocyte apoptosis after UVB exposure, whereas apoptosis was suppressed by epidermis-specific overexpression of human E2F1. Apoptosis induced by -radiation was also repressed by E2f1. E2f1-/-;Trp53-/- double knockout mice exhibited the elevated UVB-induced apoptosis of E2f1-/- alone, rather than the profound apoptosis defect seen in Trp53-/- mice, indicating that Trp53 (p53) lies functionally upstream of E2f1. Transfecting E2F1 into E2f1-/-;Trp53-/- primary fibroblasts suppressed UVB-induced apoptosis and this suppression was relieved by Trp53. The double knockout also reverted the abnormal sex ratio and early-onset tumours of Trp53-/- mice. These results imply that E2f1 functions as a suppressor of an apoptosis pathway that is initiated by DNA photoproducts and perhaps genetic abnormalities; p53 relieves this suppression.
Tárgyszavak:	idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Nature Cell Biology. - 5 : 7 (2003), p. 655-660. -
További szerzők:	Remenyik Éva (1956-) (bőrgyógyász) Knezevich, Dejan Zhang, Wengeng Liu, Ming Zhao, Hongyu Berton, T. R. Johnson, David G. Brash, Douglas E.
Internet cím:	DOI
Borító:
Saját polcon: