Zobrazeno 1 - 10
of 32
pro vyhledávání: '"Ines Pankonien"'
Autor:
Violeta Railean, Cláudia S. Rodrigues, Sofia S. Ramalho, Iris A. L. Silva, Jan Bartosch, Carlos M. Farinha, Ines Pankonien, Margarida D. Amaral
Publikováno v:
Frontiers in Molecular Biosciences, Vol 10 (2023)
Most of the 2,100 CFTR gene variants reported to date are still unknown in terms of their disease liability in Cystic Fibrosis (CF) and their molecular and cellular mechanism that leads to CFTR dysfunction. Since some rare variants may respond to cur
Externí odkaz:
https://doaj.org/article/c60cd204f58f4cc1ab638f25e1b04263
Publikováno v:
International Journal of Molecular Sciences, Vol 23, Iss 5, p 2688 (2022)
The multi-organ disease cystic fibrosis (CF) is caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR) protein, a cAMP regulated chloride (Cl−) and bicarbonate (HCO3−) ion channel expressed at the apical plasma
Externí odkaz:
https://doaj.org/article/fabce5bbafac46caa456966558e4e50f
Publikováno v:
International Journal of Molecular Sciences, Vol 21, Iss 18, p 6717 (2020)
Cystic fibrosis (CF) cells display a more cancer-like phenotype vs. non-CF cells. KLF4 overexpression has been described in CF and this transcriptional factor acts as a negative regulator of wt-CFTR. KLF4 is described as exerting its effects in a cel
Externí odkaz:
https://doaj.org/article/3d48e57edb484e7ea966cc0a625558c9
Publikováno v:
Cells, Vol 9, Iss 7, p 1607 (2020)
Cystic Fibrosis (CF) is caused by >2000 mutations in the CF transmembrane conductance regulator (CFTR) gene, but one mutation—F508del—occurs in ~80% of patients worldwide. Besides its main function as an anion channel, the CFTR protein has been i
Externí odkaz:
https://doaj.org/article/21907bc5d5b74a879ff37f6cb16cd3a8
Publikováno v:
International Journal of Molecular Sciences, Vol 21, Iss 9, p 3133 (2020)
One of the key features associated with the substantial increase in life expectancy for individuals with CF is an elevated predisposition to cancer, firmly established by recent studies involving large cohorts. With the recent advances in cystic fibr
Externí odkaz:
https://doaj.org/article/a9a7c7353da44332afa414ce348fcb19
Autor:
Margarida C Quaresma, Hugo M Botelho, Ines Pankonien, Cláudia S Rodrigues, Madalena C Pinto, Pau R Costa, Aires Duarte, Margarida D Amaral
Publikováno v:
Life science alliance. 5(9)
Mutations in the CFTR anion channel cause cystic fibrosis (CF) and have also been related to higher cancer incidence. Previously we proposed that this is linked to an emerging role of functional CFTR in protecting against epithelial–mesenchymal tra
Autor:
Luís S Sousa, Violeta Railean, Margarida C. Quaresma, Ines Pankonien, Jonas Fuxe, Tereza Doušová, Luka A. Clarke, Margarida D. Amaral, Iris A.L. Silva
Publikováno v:
Cell Death & Disease
Cell Death and Disease, Vol 11, Iss 10, Pp 1-18 (2020)
Cell Death and Disease, Vol 11, Iss 10, Pp 1-18 (2020)
Cystic fibrosis (CF) is a monogenetic disease resulting from mutations in the Cystic Fibrosis Transmembrane conductance Regulator (CFTR) gene encoding an anion channel. Recent evidence indicates that CFTR plays a role in other cellular processes, nam
Autor:
Karl Kunzelmann, Margarida D. Amaral, Iris A.L. Silva, Luís de Sousa, Luka A. Clarke, Ines Pankonien
Publikováno v:
Cells, Vol 9, Iss 1607, p 1607 (2020)
Cells
Cells; Volume 9; Issue 7; Pages: 1607
Cells
Cells; Volume 9; Issue 7; Pages: 1607
Cystic Fibrosis (CF) is caused by >2000 mutations in the CF transmembrane conductance regulator (CFTR) gene, but one mutation—F508del—occurs in ~80% of patients worldwide. Besides its main function as an anion channel, the CFTR protein has been i
Publikováno v:
International Journal of Molecular Sciences, Vol. 21, No 18 (2020) P. E6717
International Journal of Molecular Sciences
International Journal of Molecular Sciences, Vol 21, Iss 6717, p 6717 (2020)
Volume 21
Issue 18
International Journal of Molecular Sciences
International Journal of Molecular Sciences, Vol 21, Iss 6717, p 6717 (2020)
Volume 21
Issue 18
Cystic fibrosis (CF) cells display a more cancer-like phenotype vs. non-CF cells. KLF4 overexpression has been described in CF and this transcriptional factor acts as a negative regulator of wt-CFTR. KLF4 is described as exerting its effects in a cel
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8d5ef31f691ee5ff235c3a5bd1986b6c
https://archive-ouverte.unige.ch/unige:142445
https://archive-ouverte.unige.ch/unige:142445
Autor:
Veit Flockerzi, Anouar Belkacemi, Hannelore Haase, Enno Klussmann, Shimrit Oz, Nathan Dascal, Ines Pankonien
Publikováno v:
The Journal of Physiology. 595:3181-3202
β-adrenergic stimulation enhances Ca(2+) currents via L-type, voltage-gated CaV 1.2 channels, strengthening cardiac contraction. The signaling via β-adrenergic receptors (β-ARs) involves elevation of cyclic AMP (cAMP) levels and activation of prot