Nanopublications LDF server

Matches in Nanopublications for { ?s ?p "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine."@en ?g. }

• NP885708.RAlQifGaIidlJJ4IG7l_ehqjGIIP5NqFZoEDqhXKg1MCo130_assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP885708.RAlQifGaIidlJJ4IG7l_ehqjGIIP5NqFZoEDqhXKg1MCo130_provenance.
• NP615068.RApcJxetxmwtciKBDP08vWfCIYPCCgAWZ4TL8QXpLadDI130_assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP615068.RApcJxetxmwtciKBDP08vWfCIYPCCgAWZ4TL8QXpLadDI130_provenance.
• NP436767.RAdKhAcwGUDrTE2DAxcgD5j30zsiw83m0dKshPBVsQq_I130_assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP436767.RAdKhAcwGUDrTE2DAxcgD5j30zsiw83m0dKshPBVsQq_I130_provenance.
• assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
• assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
• assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
• NP669274.RAwlmg0X8gOjkAw5QlQpF-orGD-dS4YRtXqGYjwnSp1bo130_assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP669274.RAwlmg0X8gOjkAw5QlQpF-orGD-dS4YRtXqGYjwnSp1bo130_provenance.
• NP512878.RAKTtrIELaoNAVTF4EGnZBOM_sGGnz4gieFbQ8iCViRsc130_assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP512878.RAKTtrIELaoNAVTF4EGnZBOM_sGGnz4gieFbQ8iCViRsc130_provenance.
• assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
• assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
• assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
• assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
• assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
• assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." provenance.
• NP408363.RAARpuG2rvG-Ip5liYalWDAJl5YcJicxSDR-G8NUU7rOE130_assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP408363.RAARpuG2rvG-Ip5liYalWDAJl5YcJicxSDR-G8NUU7rOE130_provenance.
• NP408366.RARxJrS3QAkXwVgjbpTaBOIDVWASF2pIVaa_1PlaAey-g130_assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP408366.RARxJrS3QAkXwVgjbpTaBOIDVWASF2pIVaa_1PlaAey-g130_provenance.
• NP434922.RAmdzZ8PxbvhfPm4NiNwANqCMJkloA3IJs1_xL010F9mQ130_assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP434922.RAmdzZ8PxbvhfPm4NiNwANqCMJkloA3IJs1_xL010F9mQ130_provenance.
• NP618971.RAvUQN2Oaenwrs6snfayw_ZE9pMoxWQuHs4QnaQruG62w130_assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP618971.RAvUQN2Oaenwrs6snfayw_ZE9pMoxWQuHs4QnaQruG62w130_provenance.
• NP408367.RAgsKHzT6XXWDbX2WwJ7mQgu2gdaXQVcqZdQtOd57aEKM130_assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP408367.RAgsKHzT6XXWDbX2WwJ7mQgu2gdaXQVcqZdQtOd57aEKM130_provenance.
• NP869513.RAPMTXWkk2weJ5d5fSWe5RpRgmomN8TZBghR-6hJlGo0Q130_assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP869513.RAPMTXWkk2weJ5d5fSWe5RpRgmomN8TZBghR-6hJlGo0Q130_provenance.
• NP408362.RAK6ewltSVmo5Y84N-D3lakI0DgkWKvBHbkE2-K86OJGE130_assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP408362.RAK6ewltSVmo5Y84N-D3lakI0DgkWKvBHbkE2-K86OJGE130_provenance.
• NP408365.RAFsbMS5os03aOfee4W9RKHrrNGXfSVezjkPP3CohJiAk130_assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP408365.RAFsbMS5os03aOfee4W9RKHrrNGXfSVezjkPP3CohJiAk130_provenance.
• NP408364.RA_xYx_QSXN9GF26PStVI01YR0HoLQLX6mLdq31iD6TVM130_assertion description "[This review focuses on three key molecular mechanisms of glucocorticoid resistance in IBD: (i) decreased cytoplasmic glucocorticoid concentration secondary to increased P-glycoprotein-mediated efflux of glucocorticoid from target cells due to overexpression of the multidrug resistance gene (MDR1); (ii) impaired glucocorticoid signaling because of dysfunction at the level of the glucocorticoid receptor; and (iii) constitutive epithelial activation of proinflammatory mediators, including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine." NP408364.RA_xYx_QSXN9GF26PStVI01YR0HoLQLX6mLdq31iD6TVM130_provenance.