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  1 / 3807 MEDLINE  
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[PMID]:29287868
[Au] Autor:Chen K; Zhan Y; Wu X; Zong L; Jiang H
[Ad] Endereço:Department of Otorhinolaryngology, The First Affiliated Hospital, Sun Yat-Sen University and Institute of Otorhinolaryngology, Sun Yat-sen University, Guangzhou 510080, PR China.
[Ti] Título:Germinal mosaicism of PAX3 mutation caused Waardenburg syndrome type I.
[So] Source:Int J Pediatr Otorhinolaryngol;104:200-204, 2018 Jan.
[Is] ISSN:1872-8464
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Waardenburg syndrome mutations are most often recurrent or de novo. The rate of familial recurrence is low and families with several affected children are extremely rare. In this study, we aimed to clarify the underlying hereditary cause of Waardenburg syndrome type I in two siblings in a Chinese family, with a mother affected by prelingual mild hearing loss and a father who was negative for clinical symptoms of Waardenburg syndrome and had a normal hearing threshold. METHODS: Complete characteristic features of the family members were recorded and genetic sequencing and parent-child relationship analyses were performed. RESULTS: The two probands were found to share double mutations in the PAX3/GJB2 genes that caused concurrent hearing loss in Waardenburg syndrome type I. Their mother carried the GJB2 c.109G > A homozygous mutation; however, neither the novel PAX3 c.592delG mutation, nor the Waardenburg syndrome phenotype, was observed in either parent. CONCLUSION: These previously unreported digenic mutations in PAX3/GJB2 resulted in deafness associated with Waardenburg syndrome type I in this family. To our knowledge, this is the first report describing germinal mosaicism in Waardenburg syndrome. This concept is important because it complicates genetic counseling of this family regarding the risk of recurrence of the mutations in subsequent pregnancies.
[Mh] Termos MeSH primário: Surdez/genética
Fator de Transcrição PAX3/genética
Síndrome de Waardenburg/genética
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático/genética
Criança
Feminino
Aconselhamento Genético
Genótipo
Testes Auditivos
Homozigoto
Seres Humanos
Masculino
Mosaicismo
Mutação
Fatores de Transcrição Box Pareados/genética
Relações Pais-Filho
Linhagem
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PAX3 Transcription Factor); 0 (PAX3 protein, human); 0 (Paired Box Transcription Factors)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE


  2 / 3807 MEDLINE  
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[PMID]:28893947
[Au] Autor:Jia S; Zhou J; Fanelli C; Wee Y; Bonds J; Schneider P; Mues G; D'Souza RN
[Ad] Endereço:School of Dentistry, University of Utah, Salt Lake City, UT 84112, USA.
[Ti] Título:Small-molecule Wnt agonists correct cleft palates in mutant mice .
[So] Source:Development;144(20):3819-3828, 2017 10 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Clefts of the palate and/or lip are among the most common human craniofacial malformations and involve multiple genetic and environmental factors. Defects can only be corrected surgically and require complex life-long treatments. Our studies utilized the well-characterized mouse model with a consistent cleft palate phenotype to test small-molecule Wnt agonist therapies. We show that the absence of Pax9 alters the expression of Wnt pathway genes including and , proven antagonists of Wnt signaling. The functional interactions between Pax9 and Dkk1 are shown by the genetic rescue of secondary palate clefts in embryos. The controlled intravenous delivery of small-molecule Wnt agonists (Dkk inhibitors) into pregnant mice restored Wnt signaling and led to the growth and fusion of palatal shelves, as marked by an increase in cell proliferation and osteogenesis , while other organ defects were not corrected. This work underscores the importance of Pax9-dependent Wnt signaling in palatogenesis and suggests that this functional upstream molecular relationship can be exploited for the development of therapies for human cleft palates that arise from single-gene disorders.
[Mh] Termos MeSH primário: Fissura Palatina/genética
Fatores de Transcrição Box Pareados/genética
Palato/embriologia
Proteína Wnt1/agonistas
Proteína Wnt1/genética
[Mh] Termos MeSH secundário: Animais
Padronização Corporal
Proliferação Celular
Feminino
Perfilação da Expressão Gênica
Regulação da Expressão Gênica no Desenvolvimento
Peptídeos e Proteínas de Sinalização Intercelular/genética
Masculino
Camundongos
Camundongos Transgênicos
Morfogênese
Osteogênese
Fenótipo
Ligação Proteica
Via de Sinalização Wnt
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dkk1 protein, mouse); 0 (Dkk2 protein, mouse); 0 (Intercellular Signaling Peptides and Proteins); 0 (Paired Box Transcription Factors); 0 (Pax9 protein, mouse); 0 (Wnt1 Protein); 0 (Wnt1 protein, mouse)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.1242/dev.157750


  3 / 3807 MEDLINE  
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[PMID]:28807899
[Au] Autor:Nemec S; Luxey M; Jain D; Huang Sung A; Pastinen T; Drouin J
[Ad] Endereço:Institut de Recherches Cliniques de Montréal, Montréal, QC, H2W 1R7 Canada.
[Ti] Título: directly modulates the core limb development program to implement hindlimb identity.
[So] Source:Development;144(18):3325-3335, 2017 09 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Forelimbs (FLs) and hindlimbs (HLs) develop complex musculoskeletal structures that rely on the deployment of a conserved developmental program. , a transcription factor gene with expression restricted to HL and absent from FL, plays an important role in generating HL features. The genomic mechanisms by which effects HL identity remain poorly understood. Here, we use expression profiling and analysis of direct Pitx1 targets to characterize the HL- and FL-restricted genetic programs in mouse and situate the -dependent gene network within the context of limb-specific gene regulation. We show that is a crucial component of a narrow network of HL-restricted regulators, acting on a developmental program that is shared between FL and HL. Pitx1 targets sites that are in a similar chromatin state in FL and HL and controls expression of patterning genes as well as the chondrogenic program, consistent with impaired chondrogenesis in HL. These findings support a model in which multifactorial actions of a limited number of HL regulators redirect the generic limb development program in order to generate the unique structural features of the limb.
[Mh] Termos MeSH primário: Membro Posterior/embriologia
Membro Posterior/metabolismo
Organogênese
Fatores de Transcrição Box Pareados/metabolismo
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Condrogênese/genética
Embrião de Mamíferos/metabolismo
Elementos Facilitadores Genéticos/genética
Epigênese Genética
Membro Anterior/embriologia
Membro Anterior/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Redes Reguladoras de Genes
Loci Gênicos
Genoma
Proteínas de Homeodomínio/metabolismo
Camundongos
Organogênese/genética
Fatores de Transcrição SOX9/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Homeodomain Proteins); 0 (Paired Box Transcription Factors); 0 (SOX9 Transcription Factor); 0 (homeobox protein PITX1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.1242/dev.154864


  4 / 3807 MEDLINE  
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[PMID]:28698262
[Au] Autor:Matsuda H; Mullapudi ST; Zhang Y; Hesselson D; Stainier DYR
[Ad] Endereço:Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany hiroki.matsuda.b5@tohoku.ac.jp didier.stainier@mpi-bn.mpg.de.
[Ti] Título:Thyroid Hormone Coordinates Pancreatic Islet Maturation During the Zebrafish Larval-to-Juvenile Transition to Maintain Glucose Homeostasis.
[So] Source:Diabetes;66(10):2623-2635, 2017 Oct.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thyroid hormone (TH) signaling promotes tissue maturation and adult organ formation. Developmental transitions alter an organism's metabolic requirements, and it remains unclear how development and metabolic demands are coordinated. We used the zebrafish as a model to test whether and how TH signaling affects pancreatic islet maturation, and consequently glucose homeostasis, during the larval to juvenile transition. We found that exogenous TH precociously activates the ß-cell differentiation genes and while downregulating a master regulator of α-cell development and function. Together, these effects induced hypoglycemia, at least in part by increasing and decreasing expression. We visualized TH target tissues using a novel TH-responsive reporter line and found that both α- and ß-cells become targets of endogenous TH signaling during the larval-to-juvenile transition. Importantly, endogenous TH is required during this transition for the functional maturation of α- and ß-cells in order to maintain glucose homeostasis. Thus, our study sheds new light on the regulation of glucose metabolism during major developmental transitions.
[Mh] Termos MeSH primário: Ilhotas Pancreáticas/metabolismo
Larva/metabolismo
Hormônios Tireóideos/farmacologia
[Mh] Termos MeSH secundário: Animais
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Glucagon/genética
Glucagon/metabolismo
Glucose/metabolismo
Proteínas de Homeodomínio/genética
Proteínas de Homeodomínio/metabolismo
Insulina/genética
Insulina/metabolismo
Células Secretoras de Insulina/efeitos dos fármacos
Células Secretoras de Insulina/metabolismo
Ilhotas Pancreáticas/efeitos dos fármacos
Larva/efeitos dos fármacos
Fator de Transcrição PAX6/genética
Fator de Transcrição PAX6/metabolismo
Fatores de Transcrição Box Pareados/genética
Fatores de Transcrição Box Pareados/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Tri-Iodotironina/farmacologia
Peixe-Zebra
Proteínas de Peixe-Zebra/genética
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HB9 protein, zebrafish); 0 (Homeodomain Proteins); 0 (Insulin); 0 (PAX6 Transcription Factor); 0 (Paired Box Transcription Factors); 0 (Pax6b protein, zebrafish); 0 (Thyroid Hormones); 0 (Transcription Factors); 0 (Zebrafish Proteins); 0 (pax4 protein, zebrafish); 06LU7C9H1V (Triiodothyronine); 9007-92-5 (Glucagon); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1476


  5 / 3807 MEDLINE  
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[PMID]:28692808
[Au] Autor:Li C; Lan Y; Krumlauf R; Jiang R
[Ad] Endereço:1 Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
[Ti] Título:Modulating Wnt Signaling Rescues Palate Morphogenesis in Pax9 Mutant Mice.
[So] Source:J Dent Res;96(11):1273-1281, 2017 Oct.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cleft palate is a common birth defect caused by disruption of palatogenesis during embryonic development. Although mutations disrupting components of the Wnt signaling pathway have been associated with cleft lip and palate in humans and mice, the mechanisms involving canonical Wnt signaling and its regulation in secondary palate development are not well understood. Here, we report that canonical Wnt signaling plays an important role in Pax9-mediated regulation of secondary palate development. We found that cleft palate pathogenesis in Pax9-deficient embryos is accompanied by significantly reduced expression of Axin2, an endogenous target of canonical Wnt signaling, in the developing palatal mesenchyme, particularly in the posterior regions of the palatal shelves. We found that expression of Dkk2, encoding a secreted Wnt antagonist, is significantly increased whereas the levels of active ß-catenin protein, the essential transcriptional coactivator of canonical Wnt signaling, is significantly decreased in the posterior regions of the palatal shelves in embryonic day 13.5 Pax9-deficent embryos in comparison with control littermates. We show that small molecule-mediated inhibition of Dickkopf (DKK) activity in utero during palatal shelf morphogenesis partly rescued secondary palate development in Pax9-deficient embryos. Moreover, we found that genetic inactivation of Wise, which is expressed in the developing palatal shelves and encodes another secreted antagonist of canonical Wnt signaling, also rescued palate morphogenesis in Pax9-deficient mice. Furthermore, whereas Pax9 embryos exhibit defects in palatal shelf elevation/reorientation and significant reduction in accumulation of hyaluronic acid-a high molecular extracellular matrix glycosaminoglycan implicated in playing an important role in palatal shelf elevation-80% of Pax9 ;Wise double-mutant mouse embryos exhibit rescued palatal shelf elevation/reorientation, accompanied by restored hyaluronic acid accumulation in the palatal mesenchyme. Together, these data identify a crucial role for canonical Wnt signaling in acting downstream of Pax9 to regulate palate morphogenesis.
[Mh] Termos MeSH primário: Fissura Palatina/embriologia
Fissura Palatina/genética
Fatores de Transcrição Box Pareados/genética
Via de Sinalização Wnt/genética
[Mh] Termos MeSH secundário: Animais
Proteínas Morfogenéticas Ósseas/genética
Proliferação Celular
Desenvolvimento Embrionário
Regulação da Expressão Gênica no Desenvolvimento
Peptídeos e Proteínas de Sinalização Intercelular/genética
Camundongos
Morfogênese
Palato/embriologia
Transdução de Sinais/genética
Fatores de Transcrição/genética
Proteínas Wnt/genética
beta Catenina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Dkk2 protein, mouse); 0 (Intercellular Signaling Peptides and Proteins); 0 (Paired Box Transcription Factors); 0 (Pax9 protein, mouse); 0 (Sostdc1 protein, mouse); 0 (Transcription Factors); 0 (Wnt Proteins); 0 (beta Catenin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170711
[St] Status:MEDLINE
[do] DOI:10.1177/0022034517719865


  6 / 3807 MEDLINE  
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[PMID]:28441464
[Au] Autor:Minocha S; Boll W; Noll M
[Ad] Endereço:Institute of Molecular Life Sciences, University of Zürich, Zürich, Switzerland.
[Ti] Título:Crucial roles of Pox neuro in the developing ellipsoid body and antennal lobes of the Drosophila brain.
[So] Source:PLoS One;12(4):e0176002, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The paired box gene Pox neuro (Poxn) is expressed in two bilaterally symmetric neuronal clusters of the developing adult Drosophila brain, a protocerebral dorsal cluster (DC) and a deutocerebral ventral cluster (VC). We show that all cells that express Poxn in the developing brain are postmitotic neurons. During embryogenesis, the DC and VC consist of only 20 and 12 neurons that express Poxn, designated embryonic Poxn-neurons. The number of Poxn-neurons increases only during the third larval instar, when the DC and VC increase dramatically to about 242 and 109 Poxn-neurons, respectively, virtually all of which survive to the adult stage, while no new Poxn-neurons are added during metamorphosis. Although the vast majority of Poxn-neurons express Poxn only during third instar, about half of them are born by the end of embryogenesis, as demonstrated by the absence of BrdU incorporation during larval stages. At late third instar, embryonic Poxn-neurons, which begin to express Poxn during embryogenesis, can be easily distinguished from embryonic-born and larval-born Poxn-neurons, which begin to express Poxn only during third instar, (i) by the absence of Pros, (ii) their overt differentiation of axons and neurites, and (iii) the strikingly larger diameter of their cell bodies still apparent in the adult brain. The embryonic Poxn-neurons are primary neurons that lay out the pioneering tracts for the secondary Poxn-neurons, which differentiate projections and axons that follow those of the primary neurons during metamorphosis. The DC and the VC participate only in two neuropils of the adult brain. The DC forms most, if not all, of the neurons that connect the bulb (lateral triangle) with the ellipsoid body, a prominent neuropil of the central complex, while the VC forms most of the ventral projection neurons of the antennal lobe, which connect it ipsilaterally to the lateral horn, bypassing the mushroom bodies. In addition, Poxn-neurons of the VC are ventral local interneurons of the antennal lobe. In the absence of Poxn protein in the developing brain, embryonic Poxn-neurons stall their projections and cannot find their proper target neuropils, the bulb and ellipsoid body in the case of the DC, or the antennal lobe and lateral horn in the case of the VC, whereby the absence of the ellipsoid body neuropil is particularly striking. Poxn is thus crucial for pathfinding both in the DC and VC. Additional implications of our results are discussed.
[Mh] Termos MeSH primário: Proteínas de Drosophila/análise
Proteínas de Drosophila/genética
Drosophila melanogaster/crescimento & desenvolvimento
Regulação da Expressão Gênica no Desenvolvimento
Proteínas do Tecido Nervoso/análise
Proteínas do Tecido Nervoso/genética
Fatores de Transcrição Box Pareados/análise
Fatores de Transcrição Box Pareados/genética
[Mh] Termos MeSH secundário: Animais
Encéfalo/embriologia
Encéfalo/crescimento & desenvolvimento
Drosophila melanogaster/embriologia
Drosophila melanogaster/genética
Larva/genética
Larva/crescimento & desenvolvimento
Masculino
Mutação
Neurônios/citologia
Neurônios/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drosophila Proteins); 0 (Nerve Tissue Proteins); 0 (Paired Box Transcription Factors); 0 (Poxn protein, Drosophila)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170426
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0176002


  7 / 3807 MEDLINE  
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[PMID]:28412358
[Au] Autor:Ariyo EO; Booy EP; Dzananovic E; McRae EK; Meier M; McEleney K; Stetefeld J; McKenna SA
[Ad] Endereço:Department of Chemistry, Canada.
[Ti] Título:Impact of G-quadruplex loop conformation in the PITX1 mRNA on protein and small molecule interaction.
[So] Source:Biochem Biophys Res Commun;487(2):274-280, 2017 May 27.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intramolecular G-quadruplexes (G4s) are G-rich nucleic acid structures that fold back on themselves via interrupting loops to create stacked planar G-tetrads, in which four guanine bases associate via Hoogsteen hydrogen bonding. The G4 structure is further stabilized by monovalent cations centered between the stacked tetrads. The G-tetrad face on the top and bottom planes of G4s are often the site of interaction with proteins and small molecules. To investigate the potential impact of interrupting loops on both G4 structure and interaction with proteins/small molecules, we characterized a specific G4 from the 3'-UTR of PITX1 mRNA that contains loops of 6 nucleotides using biophysical approaches. We then introduced mutations to specific loops to determine the impact on G4 structure and the ability to interact with both proteins and a G4-specific ligand. Our results suggest that mutation of a specific loop both affects the global G4 structure and impacts the ability to interact with a G4 binding protein and small molecule ligand.
[Mh] Termos MeSH primário: Quadruplex G
MicroRNAs/química
MicroRNAs/ultraestrutura
Conformação de Ácido Nucleico
Fatores de Transcrição Box Pareados/química
Fatores de Transcrição Box Pareados/ultraestrutura
[Mh] Termos MeSH secundário: Sítios de Ligação
Simulação por Computador
MicroRNAs/genética
Modelos Químicos
Modelos Genéticos
Modelos Moleculares
Fatores de Transcrição Box Pareados/genética
Ligação Proteica
Proteínas/química
Proteínas/genética
Proteínas/ultraestrutura
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (Paired Box Transcription Factors); 0 (Proteins); 0 (homeobox protein PITX1)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170612
[Lr] Data última revisão:
170612
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170417
[St] Status:MEDLINE


  8 / 3807 MEDLINE  
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[PMID]:28375156
[Au] Autor:Bi X; Li F; Liu S; Jin Y; Zhang X; Yang T; Dai Y; Li X; Zhao AZ
[Ti] Título:ω-3 polyunsaturated fatty acids ameliorate type 1 diabetes and autoimmunity.
[So] Source:J Clin Invest;127(5):1757-1771, 2017 May 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Despite the benefit of insulin, blockade of autoimmune attack and regeneration of pancreatic islets are ultimate goals for the complete cure of type 1 diabetes (T1D). Long-term consumption of ω-3 polyunsaturated fatty acids (PUFAs) is known to suppress inflammatory processes, making these fatty acids candidates for the prevention and amelioration of autoimmune diseases. Here, we explored the preventative and therapeutic effects of ω-3 PUFAs on T1D. In NOD mice, dietary intervention with ω-3 PUFAs sharply reduced the incidence of T1D, modulated the differentiation of Th cells and Tregs, and decreased the levels of IFN-γ, IL-17, IL-6, and TNF-α. ω-3 PUFAs exerted similar effects on the differentiation of CD4+ T cells isolated from human peripheral blood mononuclear cells. The regulation of CD4+ T cell differentiation was mediated at least in part through ω-3 PUFA eicosanoid derivatives and by mTOR complex 1 (mTORC1) inhibition. Importantly, therapeutic intervention in NOD mice through nutritional supplementation or lentivirus-mediated expression of an ω-3 fatty acid desaturase, mfat-1, normalized blood glucose and insulin levels for at least 182 days, blocked the development of autoimmunity, prevented lymphocyte infiltration into regenerated islets, and sharply elevated the expression of the ß cell markers pancreatic and duodenal homeobox 1 (Pdx1) and paired box 4 (Pax4). The findings suggest that ω-3 PUFAs could potentially serve as a therapeutic modality for T1D.
[Mh] Termos MeSH primário: Autoimunidade/efeitos dos fármacos
Diabetes Mellitus Experimental/tratamento farmacológico
Diabetes Mellitus Tipo 1/tratamento farmacológico
Ácidos Graxos Ômega-3/farmacologia
[Mh] Termos MeSH secundário: Animais
Autoimunidade/genética
Glicemia/genética
Glicemia/imunologia
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/patologia
Caderinas/genética
Caderinas/imunologia
Citocinas/genética
Citocinas/imunologia
Diabetes Mellitus Experimental/genética
Diabetes Mellitus Experimental/imunologia
Diabetes Mellitus Tipo 1/genética
Diabetes Mellitus Tipo 1/imunologia
Proteínas de Homeodomínio/genética
Proteínas de Homeodomínio/imunologia
Seres Humanos
Alvo Mecanístico do Complexo 1 de Rapamicina
Camundongos
Camundongos Endogâmicos NOD
Complexos Multiproteicos/genética
Complexos Multiproteicos/imunologia
Fatores de Transcrição Box Pareados/genética
Fatores de Transcrição Box Pareados/imunologia
Serina-Treonina Quinases TOR/genética
Serina-Treonina Quinases TOR/imunologia
Transativadores/genética
Transativadores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Cadherins); 0 (Cytokines); 0 (Fath protein, mouse); 0 (Fatty Acids, Omega-3); 0 (Homeodomain Proteins); 0 (Multiprotein Complexes); 0 (Paired Box Transcription Factors); 0 (Pax4 protein, mouse); 0 (Trans-Activators); 0 (pancreatic and duodenal homeobox 1 protein); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170405
[St] Status:MEDLINE


  9 / 3807 MEDLINE  
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[PMID]:28347644
[Au] Autor:Boer EF; Van Hollebeke HF; Shapiro MD
[Ad] Endereço:Department of Biology, University of Utah, Salt Lake City, UT, USA.
[Ti] Título:Genomic determinants of epidermal appendage patterning and structure in domestic birds.
[So] Source:Dev Biol;429(2):409-419, 2017 09 15.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Variation in regional identity, patterning, and structure of epidermal appendages contributes to skin diversity among many vertebrate groups, and is perhaps most striking in birds. In pioneering work on epidermal appendage patterning, John Saunders and his contemporaries took advantage of epidermal appendage diversity within and among domestic chicken breeds to establish the importance of mesoderm-ectoderm signaling in determining skin patterning. Diversity in chickens and other domestic birds, including pigeons, is driving a new wave of research to dissect the molecular genetic basis of epidermal appendage patterning. Domestic birds are not only outstanding models for embryonic manipulations, as Saunders recognized, but they are also ideal genetic models for discovering the specific genes that control normal development and the mutations that contribute to skin diversity. Here, we review recent genetic and genomic approaches to uncover the basis of epidermal macropatterning, micropatterning, and structural variation. We also present new results that confirm expression changes in two limb identity genes in feather-footed pigeons, a case of variation in appendage structure and identity.
[Mh] Termos MeSH primário: Animais Domésticos/embriologia
Animais Domésticos/genética
Aves/embriologia
Aves/genética
Padronização Corporal/genética
Epiderme/anatomia & histologia
Epiderme/embriologia
Genoma
[Mh] Termos MeSH secundário: Animais
Plumas/fisiologia
Fatores de Transcrição Box Pareados/metabolismo
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Paired Box Transcription Factors); 0 (homeobox protein PITX1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE


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[PMID]:28302062
[Au] Autor:Scherholz M; Redl E; Wollesen T; de Oliveira AL; Todt C; Wanninger A
[Ad] Endereço:Department of Integrative Zoology, Faculty of Life Sciences, University of Vienna, Althanstraße 14, 1090, Vienna, Austria.
[Ti] Título:Ancestral and novel roles of Pax family genes in mollusks.
[So] Source:BMC Evol Biol;17(1):81, 2017 Mar 16.
[Is] ISSN:1471-2148
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Pax genes are transcription factors with significant roles in cell fate specification and tissue differentiation during animal ontogeny. Most information on their tempo-spatial mode of expression is available from well-studied model organisms where the Pax-subfamilies Pax2/5/8, Pax6, and Paxα/ß are mainly involved in the development of the central nervous system (CNS), the eyes, and other sensory organs. In certain taxa, Pax2/5/8 seems to be additionally involved in the development of excretion organs. Data on expression patterns in lophotrochozoans, and in particular in mollusks, are very scarce for all the above-mentioned Pax-subfamilies, which hampers reconstruction of their putative ancestral roles in bilaterian animals. Thus, we studied the developmental expression of Pax2/5/8, Pax6, and the lophotrochozoan-specific Paxß in the worm-shaped mollusk Wirenia argentea, a member of Aplacophora that together with Polyplacophora forms the Aculifera, the proposed sister taxon to all primarily single-shelled mollusks (Conchifera). RESULTS: All investigated Pax genes are expressed in the developing cerebral ganglia and in the ventral nerve cords, but not in the lateral nerve cords of the tetraneural nervous system. Additionally, Pax2/5/8 is expressed in epidermal spicule-secreting or associated cells of the larval trunk and in the region of the developing protonephridia. We found no indication for an involvement of the investigated Pax genes in the development of larval or adult sensory organs of Wirenia argentea. CONCLUSIONS: Pax2/5/8 seems to have a conserved role in the development of the CNS, whereas expression in the spicule-secreting tissues of aplacophorans and polyplacophorans suggests co-option in aculiferan skeletogenesis. The Pax6 expression pattern in Aculifera largely resembles the common bilaterian expression during CNS development. All data available on Paxß expression argue for a common role in lophotrochozoan neurogenesis.
[Mh] Termos MeSH primário: Moluscos/genética
Fatores de Transcrição Box Pareados/genética
Fatores de Transcrição Box Pareados/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Olho/metabolismo
Larva/crescimento & desenvolvimento
Moluscos/classificação
Moluscos/crescimento & desenvolvimento
Moluscos/metabolismo
Fatores de Transcrição Box Pareados/química
Filogenia
Alinhamento de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Paired Box Transcription Factors)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE
[do] DOI:10.1186/s12862-017-0919-x



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