Base de dados : MEDLINE
Pesquisa : D08.811.913.696.620.682.700.109 [Categoria DeCS]
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[PMID]:28468752
[Au] Autor:Zhou F; Xie F; Jin K; Zhang Z; Clerici M; Gao R; van Dinther M; Sixma TK; Huang H; Zhang L; Ten Dijke P
[Ad] Endereço:Life Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
[Ti] Título:USP4 inhibits SMAD4 monoubiquitination and promotes activin and BMP signaling.
[So] Source:EMBO J;36(11):1623-1639, 2017 06 01.
[Is] ISSN:1460-2075
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:SMAD4 is a common intracellular effector for TGF-ß family cytokines, but the mechanism by which its activity is dynamically regulated is unclear. We demonstrated that ubiquitin-specific protease (USP) 4 strongly induces activin/BMP signaling by removing the inhibitory monoubiquitination from SMAD4. This modification was triggered by the recruitment of the E3 ligase, SMURF2, to SMAD4 following ligand-induced regulatory (R)-SMAD-SMAD4 complex formation. Whereas the interaction of the negative regulator c-SKI inhibits SMAD4 monoubiquitination, the ligand stimulates the recruitment of SMURF2 to the c-SKI-SMAD2 complex and triggers c-SKI ubiquitination and degradation. Thus, SMURF2 has a role in termination and initiation of TGF-ß family signaling. An increase in monoubiquitinated SMAD4 in USP4-depleted mouse embryonic stem cells (mESCs) decreased both the BMP- and activin-induced changes in the embryonic stem cell fate. USP4 sustained SMAD4 activity during activin- and BMP-mediated morphogenic events in early zebrafish embryos. Moreover, zebrafish depleted of USP4 exhibited defective cell migration and slower coordinated cell movement known as epiboly, both of which could be rescued by SMAD4. Therefore, USP4 is a critical determinant of SMAD4 activity.
[Mh] Termos MeSH primário: Receptores de Proteínas Morfogenéticas Ósseas/metabolismo
Subunidades beta de Inibinas/metabolismo
Processamento de Proteína Pós-Traducional
Proteínas Proto-Oncogênicas/metabolismo
Transdução de Sinais
Proteína Smad4/metabolismo
Ubiquitina Tiolesterase/metabolismo
Ubiquitinação
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Movimento Celular
Células Cultivadas
Seres Humanos
Camundongos
Células-Tronco Embrionárias Murinas/fisiologia
Ubiquitina-Proteína Ligases/metabolismo
Proteases Específicas de Ubiquitina
Peixe-Zebra/embriologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins); 0 (Smad4 Protein); 0 (Smad4 protein, mouse); 0 (inhibin beta A subunit); 93443-12-0 (Inhibin-beta Subunits); EC 2.3.2.26 (Smurf2 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors); EC 3.1.2.15 (Usp4 protein, mouse); EC 3.4.19.12 (Ubiquitin Thiolesterase); EC 3.4.19.12 (Ubiquitin-Specific Proteases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180106
[Lr] Data última revisão:
180106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.15252/embj.201695372


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[PMID]:28684382
[Au] Autor:Hasegawa T; Kamada Y; Hosoya T; Fujita S; Nishiyama Y; Iwata N; Hiramatsu Y; Otsuka F
[Ad] Endereço:Departments of Obstetrics Gynecology.
[Ti] Título:A regulatory role of androgen in ovarian steroidogenesis by rat granulosa cells.
[So] Source:J Steroid Biochem Mol Biol;172:160-165, 2017 Sep.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Excess androgen and insulin-like growth factor (IGF)-I in the ovarian follicle has been suggested to be involved in the pathophysiology of polycystic ovary syndrome (PCOS). Here we investigated the impact of androgen and IGF-I on the regulatory mechanism of ovarian steroidogenesis using rat primary granulosa cells. It was revealed that androgen treatment with dihydrotestosterone (DHT) amplified progesterone synthesis in the presence of FSH and IGF-I, whereas it had no significant effect on estrogen synthesis by rat granulosa cells. In accordance with the effects of androgen on steroidogenesis, DHT enhanced the expression of progesterogenic factors and enzymes, including StAR, P450scc and 3ßHSD, and cellular cAMP synthesis induced by FSH and IGF-I. Of note, treatment with DHT and IGF-I suppressed Smad1/5/8 phosphorylation and transcription of the BMP target gene Id-1, suggesting that androgen and IGF-I counteract BMP signaling that inhibits FSH-induced progesterone synthesis in rat granulosa cells. DHT was revealed to suppress the expression of BMP-6 receptors, consisting of ALK-2, ALK-6 and ActRII, while it increased the expression of inhibitory Smads in rat granulosa cells. In addition, IGF-I treatment upregulated androgen receptor (AR) expression and DHT treatment suppressed IGF-I receptor expression on rat granulosa cells. Collectively, the results indicate that androgen and IGF-I mutually interact and accelerate progesterone production, at least in part, by regulating endogenous BMP signaling in rat granulosa cells. Cooperative effects of androgen and IGF-I counteract endogenous BMP-6 activity in rat granulosa cells, which is likely to be functionally linked to the steroidogenic property shown in the PCOS ovary.
[Mh] Termos MeSH primário: Proteína Morfogenética Óssea 1/genética
Di-Hidrotestosterona/farmacologia
Células da Granulosa/efeitos dos fármacos
Fator de Crescimento Insulin-Like I/farmacologia
Progesterona/biossíntese
[Mh] Termos MeSH secundário: Animais
Proteína Morfogenética Óssea 1/metabolismo
Receptores de Proteínas Morfogenéticas Ósseas/genética
Receptores de Proteínas Morfogenéticas Ósseas/metabolismo
AMP Cíclico/metabolismo
Sistema Enzimático do Citocromo P-450/genética
Sistema Enzimático do Citocromo P-450/metabolismo
Feminino
Hormônio Foliculoestimulante/genética
Hormônio Foliculoestimulante/metabolismo
Hormônio Foliculoestimulante/farmacologia
Regulação da Expressão Gênica
Células da Granulosa/citologia
Células da Granulosa/metabolismo
Hidroxiesteroide Desidrogenases/genética
Hidroxiesteroide Desidrogenases/metabolismo
Proteína 1 Inibidora de Diferenciação/genética
Proteína 1 Inibidora de Diferenciação/metabolismo
Fator de Crescimento Insulin-Like I/genética
Fator de Crescimento Insulin-Like I/metabolismo
Fosfoproteínas/genética
Fosfoproteínas/metabolismo
Fosforilação/efeitos dos fármacos
Cultura Primária de Células
Progesterona/agonistas
Ratos
Ratos Sprague-Dawley
Receptor IGF Tipo 1/genética
Receptor IGF Tipo 1/metabolismo
Receptores Androgênicos/genética
Receptores Androgênicos/metabolismo
Transdução de Sinais
Proteínas Smad/genética
Proteínas Smad/metabolismo
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ID1 protein, rat); 0 (Inhibitor of Differentiation Protein 1); 0 (Phosphoproteins); 0 (Receptors, Androgen); 0 (Smad Proteins); 0 (steroidogenic acute regulatory protein); 08J2K08A3Y (Dihydrotestosterone); 4G7DS2Q64Y (Progesterone); 67763-96-6 (Insulin-Like Growth Factor I); 9002-68-0 (Follicle Stimulating Hormone); 9035-51-2 (Cytochrome P-450 Enzyme System); E0399OZS9N (Cyclic AMP); EC 1.1.- (Hydroxysteroid Dehydrogenases); EC 2.7.10.1 (Receptor, IGF Type 1); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors); EC 3.4.24.19 (Bone Morphogenetic Protein 1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE


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[PMID]:28642261
[Au] Autor:Zhang H; Du L; Zhong Y; Flanders KC; Roberts JD
[Ad] Endereço:Cardiovascular Research Center of the General Medical Services, Massachusetts General Hospital, Boston, Massachusetts.
[Ti] Título:Transforming growth factor-ß stimulates Smad1/5 signaling in pulmonary artery smooth muscle cells and fibroblasts of the newborn mouse through ALK1.
[So] Source:Am J Physiol Lung Cell Mol Physiol;313(3):L615-L627, 2017 Sep 01.
[Is] ISSN:1522-1504
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The intracellular signaling mechanisms through which TGF-ß regulates pulmonary development are incompletely understood. Canonical TGF-ß signaling involves Smad2/3 phosphorylation, Smad2/3·Smad4 complex formation and nuclear localization, and gene regulation. Here, we show that physiologically relevant TGF-ß1 levels also stimulate Smad1/5 phosphorylation, which is typically a mediator of bone morphogenetic protein (BMP) signaling, in mouse pup pulmonary artery smooth muscle cells (mPASMC) and lung fibroblasts and other interstitial lung cell lines. This cross-talk mechanism likely has in vivo relevance because mixed Smad1/5/8·Smad2/3 complexes, which are indicative of TGF-ß-stimulated Smad1/5 activation, were detected in the developing mouse lung using a proximity ligation assay. Although mixed Smad complexes have been shown not to transduce nuclear signaling, we determined that TGF-ß stimulates nuclear localization of phosphorylated Smad1/5 and induces the expression of prototypical BMP-regulated genes in the mPASMC. Small-molecule kinase inhibitor studies suggested that TGF-ß-regulated Smad1/5 phosphorylation in these cells is mediated by TGF-ß-type I receptors, not BMP-type I receptors, but possibly the accessory activin-like kinase (ALK1) receptor. Although work by others suggested that ALK1 is expressed exclusively in endothelial cells in the vasculature, we detected ALK1 mRNA and protein expression in mPASMC in vitro and in mouse pup lungs. Moreover, using an antimurine ALK1 antibody and mPASMC, we determined that ALK1 regulates Smad1/5 phosphorylation by TGF-ß. Together, these studies characterize an accessory TGF-ß-stimulated BMP R-Smad signaling mechanism in interstitial cells of the developing lung. They also indicate the importance of considering alternate Smad pathways in studies directed at determining how TGF-ß regulates newborn lung development.
[Mh] Termos MeSH primário: Receptores de Ativinas Tipo I/metabolismo
Fibroblastos/metabolismo
Miócitos de Músculo Liso/metabolismo
Artéria Pulmonar/citologia
Transdução de Sinais/efeitos dos fármacos
Proteína Smad1/metabolismo
Proteína Smad5/metabolismo
Fator de Crescimento Transformador beta/farmacologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Benzodioxóis/farmacologia
Receptores de Proteínas Morfogenéticas Ósseas/metabolismo
Linhagem Celular
Núcleo Celular/efeitos dos fármacos
Núcleo Celular/metabolismo
Seres Humanos
Imidazóis/farmacologia
Pulmão/crescimento & desenvolvimento
Pulmão/metabolismo
Camundongos
Miócitos de Músculo Liso/efeitos dos fármacos
Fosforilação/efeitos dos fármacos
Proteínas Serina-Treonina Quinases/metabolismo
Piridinas/farmacologia
Ratos
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(5-benzo(1,3)dioxol-5-yl-2-tert-butyl-3H-imidazol-4-yl)-6-methylpyridine hydrochloride); 0 (Benzodioxoles); 0 (Imidazoles); 0 (Pyridines); 0 (Receptors, Transforming Growth Factor beta); 0 (Smad1 Protein); 0 (Smad5 Protein); 0 (Transforming Growth Factor beta); EC 2.7.1.11 (TGF-beta type I receptor); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.30 (Activin Receptors, Type I); EC 2.7.11.30 (Acvr1 protein, mouse); EC 2.7.11.30 (Acvrl1 protein, mouse); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170624
[St] Status:MEDLINE
[do] DOI:10.1152/ajplung.00079.2017


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[PMID]:28202676
[Au] Autor:Bosukonda A; Carlson WD
[Ad] Endereço:Albany Medical College, Albany, NY, U.S.A.
[Ti] Título:Harnessing the BMP signaling pathway to control the formation of cancer stem cells by effects on epithelial-to-mesenchymal transition.
[So] Source:Biochem Soc Trans;45(1):223-228, 2017 Feb 08.
[Is] ISSN:1470-8752
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cancer stem cells (CSCs) persist in tumors as a distinct population and may be causative in metastasis and relapse. CSC-rich tumors are associated with higher rates of metastasis and poor patient prognosis. Targeting CSCs therapeutically is challenging, since they seem to be resistant to standard chemotherapy. We have shown that a novel peptide agonist of bone morphogenetic protein (BMP) signaling, P123, is capable of inhibiting the growth of primary tumor cells by interacting with type I receptors selectively [activin receptor-like kinase 2 (ALK2) and ALK3, but not ALK6] and type II BMP receptors, activating SMAD 1/5/8 signaling and controlling the cell cycle pathway. Furthermore, the compound is capable of blocking transforming growth factor-ß induced epithelial-to-mesenchymal transition (EMT) in primary tumor cells, a critical step for tumor progression and metastasis. In addition, we have investigated the effects of P123 on self-renewal, growth, differentiation (reversal of EMT) and apoptosis of isolated human breast CSCs. We have shown that P123 and BMP-7 reverse the EMT process in human breast CSCs, and inhibit self-renewal and growth. Moreover, compared with single treatment with paclitaxel, co-treatment with paclitaxel and P123 showed an increase in cell apoptosis. Together, these findings suggest that P123 has the therapeutic potential to suppress both bulk tumor cells and CSCs. We believe that P123 represents a new class of drugs that have the potential to eliminate the primary tumor, prevent reoccurrence and metastasis, and enhance the treatment of breast cancer.
[Mh] Termos MeSH primário: Proteínas Morfogenéticas Ósseas/metabolismo
Transição Epitelial-Mesenquimal
Células-Tronco Neoplásicas/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Receptores de Ativinas/metabolismo
Receptores de Ativinas Tipo I
Antineoplásicos Fitogênicos/farmacologia
Apoptose/efeitos dos fármacos
Proteína Morfogenética Óssea 7/agonistas
Proteína Morfogenética Óssea 7/metabolismo
Receptores de Proteínas Morfogenéticas Ósseas/metabolismo
Proteínas Morfogenéticas Ósseas/agonistas
Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Feminino
Seres Humanos
Células MCF-7
Células-Tronco Neoplásicas/efeitos dos fármacos
Paclitaxel/farmacologia
Peptídeos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Bone Morphogenetic Protein 7); 0 (Bone Morphogenetic Proteins); 0 (Peptides); EC 2.7.11.30 (ACVR1B protein, human); EC 2.7.11.30 (Activin Receptors); EC 2.7.11.30 (Activin Receptors, Type I); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors); P88XT4IS4D (Paclitaxel)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170721
[Lr] Data última revisão:
170721
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170217
[St] Status:MEDLINE
[do] DOI:10.1042/BST20160177


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[PMID]:28202671
[Au] Autor:Sedlmeier G; Sleeman JP
[Ad] Endereço:Centre for Biomedicine and Medical Technology Mannheim, Medical Faculty Mannheim, University Heidelberg, 68167 Mannheim, Germany georg.sedlmeier@medma.uni-heidelberg.de jonathan.sleeman@medma.uni-heidelberg.de.
[Ti] Título:Extracellular regulation of BMP signaling: welcome to the matrix.
[So] Source:Biochem Soc Trans;45(1):173-181, 2017 Feb 08.
[Is] ISSN:1470-8752
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Given its importance in development and homeostasis, bone morphogenetic protein (BMP) signaling is tightly regulated at the extra- and intracellular level. The extracellular matrix (ECM) was initially thought to act as a passive mechanical barrier that sequesters BMPs. However, a new understanding about how the ECM plays an instructive role in regulating BMP signaling is emerging. In this mini-review, we discuss various ways in which the biochemical and physical properties of the ECM regulate BMP signaling.
[Mh] Termos MeSH primário: Proteínas Morfogenéticas Ósseas/metabolismo
Matriz Extracelular/metabolismo
Espaço Extracelular/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Receptores de Proteínas Morfogenéticas Ósseas/metabolismo
Proteínas da Matriz Extracelular/metabolismo
Homeostase
Seres Humanos
Modelos Biológicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Extracellular Matrix Proteins); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170721
[Lr] Data última revisão:
170721
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170217
[St] Status:MEDLINE
[do] DOI:10.1042/BST20160263


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[PMID]:27815159
[Au] Autor:Rajesh G; Paul A; Mishra SR; Bharati J; Thakur N; Mondal T; Soren S; Harikumar S; Narayanan K; Chouhan VS; Bag S; Das BC; Singh G; Maurya VP; Sharma GT; Sarkar M
[Ad] Endereço:Physiology & Climatology Division, Indian Veterinary Research Institute, Izatnagar, Uttar Pradesh 243122, India.
[Ti] Título:Expression and functional role of Bone Morphogenetic Proteins (BMPs) in cyclical corpus luteum in buffalo (Bubalus bubalis).
[So] Source:Gen Comp Endocrinol;240:198-213, 2017 Jan 01.
[Is] ISSN:1095-6840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The role of growth factors in the modulation of ovarian function is an interesting area of research in reproductive biology. Recently, we have shown the expression and role of IGF, EGF, VEGF and FGF in the follicle and CL. Here, we report the presence of Bone Morphogenetic Proteins (BMPs) and their functional receptors in the corpus luteum (CL) of buffalo. The bubaline CL was classified into four stages according to the morphology and progesterone (P ) concentration. The qPCR, immunoblot and immunohistochemistry studies revealed that BMP2 and BMP Receptors (BMPR1A, BMPR1B and BMPR2) were significantly upregulated during the mid stage whereas BMP4 and BMP7 were upregulated during the early stage of CL (P<0.05). Studies on primary luteal cell culture (LCC) using mid CL showed a significant time and concentration dependent effect of BMP4 and BMP7 (P<0.05). At 100ngml , the BMPs maximally stimulated the transcripts of StAR, CYP11A1 and 3ßHSD that paralleled with P accretion in the media (P<0.05). Further, the BMP4 as well as BMP7 upregulated the transcripts of PCNA and downregulated CASPASE3 in the LCC at the same concentration (P<0.05). Though the combined effect of BMP4 and 7 was significantly higher (P<0.05) than that of individual one, it was not additive. In conclusion, the expression of BMPs and their receptors were dependent on the stages of CL in the buffalo. Treatment of LCC with BMPs in vitro confirmed the presence of functional receptors that stimulated the P production and luteal cell survival. Moreover, the results support the concept that the upregulation of P and its biosynthetic pathway enzymes such as CYP11A1, StAR and 3ßHSD in the CL is likely due to the autocrine and /or paracrine effects of BMP4 and BMP7 under physiological milieu.
[Mh] Termos MeSH primário: Proteínas Morfogenéticas Ósseas/genética
Búfalos/genética
Corpo Lúteo/metabolismo
Regulação da Expressão Gênica
[Mh] Termos MeSH secundário: Animais
Apoptose
Receptores de Proteínas Morfogenéticas Ósseas/metabolismo
Proteínas Morfogenéticas Ósseas/metabolismo
Caspase 3/genética
Caspase 3/metabolismo
Células Cultivadas
Feminino
Perfilação da Expressão Gênica
Immunoblotting
Imuno-Histoquímica
Progesterona/genética
Progesterona/metabolismo
Antígeno Nuclear de Célula em Proliferação/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Proliferating Cell Nuclear Antigen); 0 (RNA, Messenger); 4G7DS2Q64Y (Progesterone); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161106
[St] Status:MEDLINE


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[PMID]:27803996
[Au] Autor:Iyer S; Chhabra Y; Harvey TJ; Wang R; Chiu HS; Smith AG; Thomas WG; Pennisi DJ; Piper M
[Ad] Endereço:School of Biomedical Sciences, The University of Queensland, Brisbane, 4072, Australia.
[Ti] Título:CRIM1 is necessary for coronary vascular endothelial cell development and homeostasis.
[So] Source:J Mol Histol;48(1):53-61, 2017 Feb.
[Is] ISSN:1567-2387
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Endothelial cells form a critical component of the coronary vasculature, yet the factors regulating their development remain poorly defined. Here we reveal a novel role for the transmembrane protein CRIM1 in mediating cardiac endothelial cell development. In the absence of Crim1 in vivo, the coronary vasculature is malformed, the number of endothelial cells reduced, and the canonical BMP pathway dysregulated. Moreover, we reveal that CRIM1 can bind IGFs, and regulate IGF signalling within endothelial cells. Finally, loss of CRIM1 from human cardiac endothelial cells results in misregulation of endothelial genes, predicted by pathway analysis to be involved in an increased inflammatory response and cytolysis, reminiscent of endothelial cell dysfunction in cardiovascular disease pathogenesis. Collectively, these findings implicate CRIM1 in endothelial cell development and homeostasis in the coronary vasculature.
[Mh] Termos MeSH primário: Receptores de Proteínas Morfogenéticas Ósseas/genética
Receptores de Proteínas Morfogenéticas Ósseas/metabolismo
Vasos Coronários/citologia
Células Endoteliais/metabolismo
Homeostase
[Mh] Termos MeSH secundário: Animais
Proteínas Morfogenéticas Ósseas/metabolismo
Sobrevivência Celular/genética
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Camundongos
Camundongos Knockout
Mutação
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Crim1 protein, mouse); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161103
[St] Status:MEDLINE
[do] DOI:10.1007/s10735-016-9702-3


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[PMID]:28359351
[Au] Autor:Zhang Y; Liu Y; Hang A; Phan E; Wildsoet CF
[Ad] Endereço:Center for Eye Disease & Development,School of Optometry,University of California,Berkeley,CA,USA.
[Ti] Título:Differential gene expression of BMP2 and BMP receptors in chick retina & choroid induced by imposed optical defocus.
[So] Source:Vis Neurosci;33:E015, 2016 01.
[Is] ISSN:1469-8714
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Recent studies have demonstrated the defocus sign-dependent, bidirectional gene expression regulation of bone morphogenetic proteins, BMP2, 4 and 7 in chick RPE. In this study, we examined the effects of imposed positive (+10 D) and negative (-10 D) lenses on the gene expression of these BMPs and BMP receptors (BMPR1A, BMPR1B, BMPR2) in chick retina and choroid after monocular lens treatment for 2 or 48 h, as indicators of the roles of retinal and choroidal BMPs and receptors in postnatal eye growth regulation. In retina, although all genes were expressed, neither +10 nor -10 D lenses, worn for either 2 or 48 h, significantly altered gene expression. In contrast, treatment-related differential gene expression was detected in the choroid for both BMPs and their receptors, although interestingly, with the +10 D lens, BMP2 was up-regulated by 156.7 ± 19.7% after 2 h, while BMPR1A was down-regulated to 82.3 ± 12.5% only after 48 h. With the -10 D lens, only the gene expression of BMPR1B was significantly altered, being up-regulated by 162.3 ± 21.2% after 48 h. Untreated birds showed no difference in expression between their two eyes, for any of the genes examined. The finding that retinal gene expression for BMP2, 4, 7 and their receptors are not affected by short-term optical defocus contrasts with previous observations of sign-dependent expression changes for the same genes in the RPE. The latter changes were also larger and more consistent in direction than the choroidal gene expression changes reported here. The interrelationship between these various changes and their biological significance for eye growth regulation are yet to be elucidated.
[Mh] Termos MeSH primário: Proteína Morfogenética Óssea 2/genética
Receptores de Proteínas Morfogenéticas Ósseas/genética
Corioide/metabolismo
Modelos Animais de Doenças
Regulação da Expressão Gênica/fisiologia
Miopia/genética
Retina/metabolismo
[Mh] Termos MeSH secundário: Animais
Comprimento Axial do Olho/patologia
Galinhas
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Bone Morphogenetic Protein 2); 0 (RNA, Messenger); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170401
[St] Status:MEDLINE
[do] DOI:10.1017/S0952523816000122


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[PMID]:27814354
[Au] Autor:Gui J; Huang Y; Shimmi O
[Ad] Endereço:Institute of Biotechnology, University of Helsinki, Helsinki, Finland.
[Ti] Título:Scribbled Optimizes BMP Signaling through Its Receptor Internalization to the Rab5 Endosome and Promote Robust Epithelial Morphogenesis.
[So] Source:PLoS Genet;12(11):e1006424, 2016 Nov.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epithelial cells are characterized by apical-basal polarity. Intrinsic factors underlying apical-basal polarity are crucial for tissue homeostasis and have often been identified to be tumor suppressors. Patterning and differentiation of epithelia are key processes of epithelial morphogenesis and are frequently regulated by highly conserved extrinsic factors. However, due to the complexity of morphogenesis, the mechanisms of precise interpretation of signal transduction as well as spatiotemporal control of extrinsic cues during dynamic morphogenesis remain poorly understood. Wing posterior crossvein (PCV) formation in Drosophila serves as a unique model to address how epithelial morphogenesis is regulated by secreted growth factors. Decapentaplegic (Dpp), a conserved bone morphogenetic protein (BMP)-type ligand, is directionally trafficked from longitudinal veins (LVs) into the PCV region for patterning and differentiation. Our data reveal that the basolateral determinant Scribbled (Scrib) is required for PCV formation through optimizing BMP signaling. Scrib regulates BMP-type I receptor Thickveins (Tkv) localization at the basolateral region of PCV cells and subsequently facilitates Tkv internalization to Rab5 endosomes, where Tkv is active. BMP signaling also up-regulates scrib transcription in the pupal wing to form a positive feedback loop. Our data reveal a unique mechanism in which intrinsic polarity genes and extrinsic cues are coupled to promote robust morphogenesis.
[Mh] Termos MeSH primário: Proteínas de Drosophila/genética
Morfogênese/genética
Proteínas Serina-Treonina Quinases/genética
Receptores de Superfície Celular/genética
Proteínas Supressoras de Tumor/genética
Proteínas rab5 de Ligação ao GTP/genética
[Mh] Termos MeSH secundário: Animais
Receptores de Proteínas Morfogenéticas Ósseas/genética
Proteínas Morfogenéticas Ósseas/genética
Proteínas Morfogenéticas Ósseas/metabolismo
Diferenciação Celular/genética
Polaridade Celular/genética
Drosophila melanogaster/genética
Drosophila melanogaster/crescimento & desenvolvimento
Endossomos/genética
Endossomos/metabolismo
Epitélio/crescimento & desenvolvimento
Epitélio/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Transporte Proteico/genética
Asas de Animais/crescimento & desenvolvimento
Asas de Animais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Drosophila Proteins); 0 (Receptors, Cell Surface); 0 (Tumor Suppressor Proteins); 0 (dpp protein, Drosophila); 0 (scribbled protein, Drosophila); EC 2.7.1.- (tkv protein, Drosophila); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors); EC 3.6.1.47. (Rab5 protein, Drosophila); EC 3.6.5.2 (rab5 GTP-Binding Proteins)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170501
[Lr] Data última revisão:
170501
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006424


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[PMID]:27703004
[Au] Autor:Baas R; Sijm A; van Teeffelen HA; van Es R; Vos HR; Marc Timmers HT
[Ad] Endereço:From the Departments of Molecular Cancer Research and Stem Cells, Regenerative Medicine Center, Center for Molecular Medicine, University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands.
[Ti] Título:Quantitative Proteomics of the SMAD (Suppressor of Mothers against Decapentaplegic) Transcription Factor Family Identifies Importin 5 as a Bone Morphogenic Protein Receptor SMAD-specific Importin.
[So] Source:J Biol Chem;291(46):24121-24132, 2016 Nov 11.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gene-specific transcription factors (GSTFs) control gene transcription by DNA binding and specific protein complex recruitment, which regulates promoter accessibility for transcription initiation by RNA polymerase II. Mutations in the GSTFs Suppressor of Mothers Against Decapentaplegic 2 (SMAD2) and SMAD4 are frequently associated with colon and rectal carcinomas. These proteins play an important role in bone morphogenic protein (BMP) and transforming growth factor ß (TGF-ß) signaling pathways controlling cell fate and proliferation. To study the protein interactome of the SMAD protein family we generated a quantitative proteomics pipeline that allows for inducible expression of GFP-tagged SMAD proteins followed by affinity purification and quantitative mass spectrometry analysis. Data are available via ProteomeXchange with identifier PXD004529. The nuclear importin IPO5 was identified as a novel interacting protein of SMAD1. Overexpression of IPO5 in various cell lines specifically increases nuclear localization of BMP receptor-activated SMADs (R-SMADs) confirming a functional relationship between IPO5 and BMP but not TGF-ß R-SMADs. Finally, we provide evidence that variation in length of the lysine stretch of the nuclear localization sequence is a determinant for importin specificity.
[Mh] Termos MeSH primário: Núcleo Celular/metabolismo
Proteína Smad1/metabolismo
Proteína Smad2/metabolismo
Proteína Smad4/metabolismo
beta Carioferinas/metabolismo
[Mh] Termos MeSH secundário: Receptores de Proteínas Morfogenéticas Ósseas/genética
Receptores de Proteínas Morfogenéticas Ósseas/metabolismo
Núcleo Celular/genética
Células HeLa
Seres Humanos
Proteômica
Proteína Smad1/genética
Proteína Smad2/genética
Proteína Smad4/genética
beta Carioferinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IPO5 protein, human); 0 (SMAD1 protein, human); 0 (SMAD2 protein, human); 0 (SMAD4 protein, human); 0 (Smad1 Protein); 0 (Smad2 Protein); 0 (Smad4 Protein); 0 (beta Karyopherins); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161006
[St] Status:MEDLINE



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