Ino Fraga Filho (Federal University of Rio de Janeiro, Brazil) for providing buffycoats, and the NIH AIDS Research and Reference Reagent Program (Division of AIDS, NIAID, NIH, Bethesda, MD) for providing the HIV-1 isolate Ba-L. The recombinant protein Maxadilan and its truncated form MaxadilanD65 (M65) were kindly donated to us by Dr. Ethan A. Lerner (Department of Dermatology, Massachusetts General Hospital, MA, USA).Author ContributionsConceived and designed the experiments: JRT EGR WS DCBH. Performed the experiments: JRT RJ EGR. Analyzed the data: JRT WS DCBH. Wrote the paper: JRT WS DCBH.VIP and PACAP Inhibit HIV-1 Infection
High Mobility Group A proteins (HMGA1a, HMGA1b and HMGA2) are chromatin architectural factors involved in embryonic development and neoplastic transformation. HMGA are typically 80-49-9 manufacturer characterized by three highly conserved short basic DNA binding domains (AT-hooks) and a constitutively phosphorylated acidic C-terminal tail that is involved in modulating HMGA interactivity and conformation [1]. HMGA are architectural chromatin modifiers because by binding to DNA they can affect its structure, and by interacting with other nuclear proteins they can participate in the assembling of complexes involved in regulating the expression of several genes that are crucial for cell growth, proliferation, and differentiation [2,3]. HMGA are highly expressed during embryogenesis, but their expression is low or undetectable in fully differentiated adult tissues; however, after neoplastic transformation, HMGA are heavily re-expressed [3?]. Several evidences suggest a role for both genes in cell proliferation and differentiation. Hmga2 knockdown in Xenopus 3PO chemical information laevis abrogates in vivo cardiogenesis [7]. Hmga2 knockout in mice leads to the pygmy phenotype, characterized by reduced body size due to a decrease in mesenchymal cell proliferation [8] and by a deficit in myoblast proliferation and in myogenesis [9]; besides, these mice are sterile because of impaired testis maturation [10] and are affected innormal neural stem cell self-renewal [11]. In mice, haploinsufficiency of the Hmga1 gene causes cardiac hypertrophy and myelolymphoproliferative disorders [12]; besides, Hmga1 is required for normal sperm development and a role for both Hmga1 and Hmga2 genes has been demonstrated in adipogenesis [10]. In humans, HMGA2 haploinsufficiency is associated with growth retardation and reduced height [13,14]. Altogether these reports underline an involvement of HMGA 23727046 in development and in cell commitment. We and others have previously reported the identification and developmental expression of Xenopus laevis hmga2 [7,15,16]; we here report the identification of a new multi-AT-hook factor, that we named XHMG-AT-hook, whose biochemical properties differ from those of the HMGA family, suggesting that it might have different functions. We describe its developmental expression pattern and show that its knock-down in anterior regions results in abnormal development of the eye and of the neural crest cell (NCC) derived pharyngeal skeleton.Materials and MethodsAll animal work has been conducted according to relevant national and international guidelines. In particular, all protocols involving the use of animals were approved by the BioethicalMulti-AT-Hook Factors in XenopusCommittee of Pisa University, according to EU Directive 2010/ 63/ EU.Computational Analysis of DNAA search in the database for proteins homologous to human HMGA1, using the TBLASTN tool as d.Ino Fraga Filho (Federal University of Rio de Janeiro, Brazil) for providing buffycoats, and the NIH AIDS Research and Reference Reagent Program (Division of AIDS, NIAID, NIH, Bethesda, MD) for providing the HIV-1 isolate Ba-L. The recombinant protein Maxadilan and its truncated form MaxadilanD65 (M65) were kindly donated to us by Dr. Ethan A. Lerner (Department of Dermatology, Massachusetts General Hospital, MA, USA).Author ContributionsConceived and designed the experiments: JRT EGR WS DCBH. Performed the experiments: JRT RJ EGR. Analyzed the data: JRT WS DCBH. Wrote the paper: JRT WS DCBH.VIP and PACAP Inhibit HIV-1 Infection
High Mobility Group A proteins (HMGA1a, HMGA1b and HMGA2) are chromatin architectural factors involved in embryonic development and neoplastic transformation. HMGA are typically characterized by three highly conserved short basic DNA binding domains (AT-hooks) and a constitutively phosphorylated acidic C-terminal tail that is involved in modulating HMGA interactivity and conformation [1]. HMGA are architectural chromatin modifiers because by binding to DNA they can affect its structure, and by interacting with other nuclear proteins they can participate in the assembling of complexes involved in regulating the expression of several genes that are crucial for cell growth, proliferation, and differentiation [2,3]. HMGA are highly expressed during embryogenesis, but their expression is low or undetectable in fully differentiated adult tissues; however, after neoplastic transformation, HMGA are heavily re-expressed [3?]. Several evidences suggest a role for both genes in cell proliferation and differentiation. Hmga2 knockdown in Xenopus laevis abrogates in vivo cardiogenesis [7]. Hmga2 knockout in mice leads to the pygmy phenotype, characterized by reduced body size due to a decrease in mesenchymal cell proliferation [8] and by a deficit in myoblast proliferation and in myogenesis [9]; besides, these mice are sterile because of impaired testis maturation [10] and are affected innormal neural stem cell self-renewal [11]. In mice, haploinsufficiency of the Hmga1 gene causes cardiac hypertrophy and myelolymphoproliferative disorders [12]; besides, Hmga1 is required for normal sperm development and a role for both Hmga1 and Hmga2 genes has been demonstrated in adipogenesis [10]. In humans, HMGA2 haploinsufficiency is associated with growth retardation and reduced height [13,14]. Altogether these reports underline an involvement of HMGA 23727046 in development and in cell commitment. We and others have previously reported the identification and developmental expression of Xenopus laevis hmga2 [7,15,16]; we here report the identification of a new multi-AT-hook factor, that we named XHMG-AT-hook, whose biochemical properties differ from those of the HMGA family, suggesting that it might have different functions. We describe its developmental expression pattern and show that its knock-down in anterior regions results in abnormal development of the eye and of the neural crest cell (NCC) derived pharyngeal skeleton.Materials and MethodsAll animal work has been conducted according to relevant national and international guidelines. In particular, all protocols involving the use of animals were approved by the BioethicalMulti-AT-Hook Factors in XenopusCommittee of Pisa University, according to EU Directive 2010/ 63/ EU.Computational Analysis of DNAA search in the database for proteins homologous to human HMGA1, using the TBLASTN tool as d.
