something to replace cftr

P

petersymons

Guest
This is an interesting little article on something to possibly replace the role of the cftr.

Cancer Lett. 2010 Jun 28;292(2):246-53. Epub 2010 Jan 20.
Tobacco carcinogen NNK transporter MRP2 regulates CFTR function in lung epithelia: implications for lung cancer.
Li C, Schuetz JD, Naren AP.

Department of Biochemistry and Molecular Biology, Wayne State University School of Medicine, 540 E. Canfield Avenue, 5312 Scott Hall, Detroit, MI 48201, USA.
Abstract
Lung cancer is the leading cause of cancer death in the United States. About 85% of all lung cancers are linked to tobacco smoke, in which more than 50 lung carcinogens have been identified and one of the most abundant is 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). The human lung epithelium constitutes the first line of defense against tobacco-specific carcinogens, in which apically-localized receptors, transporters, and ion channels in the airway may play a critical role in this native defense against tobacco smoke. Here we showed that multidrug resistance protein-2 (MRP2) and cystic fibrosis transmembrane conductance regulator (CFTR), two ATP-binding cassette (ABC) transporters, are localized to the apical surfaces of plasma membrane in polarized lung epithelial cells. We observed that there is a functional coupling between CFTR and MRP2 that may be mediated by PDZ proteins. We also observed the existence of a macromolecular complex containing CFTR, MRP2, and PDZ proteins, which might form the basis for the regulatory cooperation between these two ABC transporters. Our results have important implications for cigarette smoke-associated lung diseases (such as smoke-related emphysema, chronic obstructive pulmonary disease, and lung cancer). Copyright 2009 Elsevier Ireland Ltd. All rights reserved.

PMID: 20089353 [PubMed - indexed for MEDLINE]PMCID: PMC2868381 [Available on 2011/6/28]

Publication Types, MeSH Terms, Substances, Grant Support
LinkOut - more resources
 
P

petersymons

Guest
This is an interesting little article on something to possibly replace the role of the cftr.

Cancer Lett. 2010 Jun 28;292(2):246-53. Epub 2010 Jan 20.
Tobacco carcinogen NNK transporter MRP2 regulates CFTR function in lung epithelia: implications for lung cancer.
Li C, Schuetz JD, Naren AP.

Department of Biochemistry and Molecular Biology, Wayne State University School of Medicine, 540 E. Canfield Avenue, 5312 Scott Hall, Detroit, MI 48201, USA.
Abstract
Lung cancer is the leading cause of cancer death in the United States. About 85% of all lung cancers are linked to tobacco smoke, in which more than 50 lung carcinogens have been identified and one of the most abundant is 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). The human lung epithelium constitutes the first line of defense against tobacco-specific carcinogens, in which apically-localized receptors, transporters, and ion channels in the airway may play a critical role in this native defense against tobacco smoke. Here we showed that multidrug resistance protein-2 (MRP2) and cystic fibrosis transmembrane conductance regulator (CFTR), two ATP-binding cassette (ABC) transporters, are localized to the apical surfaces of plasma membrane in polarized lung epithelial cells. We observed that there is a functional coupling between CFTR and MRP2 that may be mediated by PDZ proteins. We also observed the existence of a macromolecular complex containing CFTR, MRP2, and PDZ proteins, which might form the basis for the regulatory cooperation between these two ABC transporters. Our results have important implications for cigarette smoke-associated lung diseases (such as smoke-related emphysema, chronic obstructive pulmonary disease, and lung cancer). Copyright 2009 Elsevier Ireland Ltd. All rights reserved.

PMID: 20089353 [PubMed - indexed for MEDLINE]PMCID: PMC2868381 [Available on 2011/6/28]

Publication Types, MeSH Terms, Substances, Grant Support
LinkOut - more resources
 
P

petersymons

Guest
This is an interesting little article on something to possibly replace the role of the cftr.
<br />
<br />Cancer Lett. 2010 Jun 28;292(2):246-53. Epub 2010 Jan 20.
<br />Tobacco carcinogen NNK transporter MRP2 regulates CFTR function in lung epithelia: implications for lung cancer.
<br />Li C, Schuetz JD, Naren AP.
<br />
<br />Department of Biochemistry and Molecular Biology, Wayne State University School of Medicine, 540 E. Canfield Avenue, 5312 Scott Hall, Detroit, MI 48201, USA.
<br />Abstract
<br />Lung cancer is the leading cause of cancer death in the United States. About 85% of all lung cancers are linked to tobacco smoke, in which more than 50 lung carcinogens have been identified and one of the most abundant is 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). The human lung epithelium constitutes the first line of defense against tobacco-specific carcinogens, in which apically-localized receptors, transporters, and ion channels in the airway may play a critical role in this native defense against tobacco smoke. Here we showed that multidrug resistance protein-2 (MRP2) and cystic fibrosis transmembrane conductance regulator (CFTR), two ATP-binding cassette (ABC) transporters, are localized to the apical surfaces of plasma membrane in polarized lung epithelial cells. We observed that there is a functional coupling between CFTR and MRP2 that may be mediated by PDZ proteins. We also observed the existence of a macromolecular complex containing CFTR, MRP2, and PDZ proteins, which might form the basis for the regulatory cooperation between these two ABC transporters. Our results have important implications for cigarette smoke-associated lung diseases (such as smoke-related emphysema, chronic obstructive pulmonary disease, and lung cancer). Copyright 2009 Elsevier Ireland Ltd. All rights reserved.
<br />
<br />PMID: 20089353 [PubMed - indexed for MEDLINE]PMCID: PMC2868381 [Available on 2011/6/28]
<br />
<br />Publication Types, MeSH Terms, Substances, Grant Support
<br />LinkOut - more resources
 
P

petersymons

Guest
There is a group working on something to maybe have mrp2 do some of the work of the cftr.
 
P

petersymons

Guest
There is a group working on something to maybe have mrp2 do some of the work of the cftr.
 
P

petersymons

Guest
There is a group working on something to maybe have mrp2 do some of the work of the cftr.
 
P

petersymons

Guest
static the thought is that what is meant to be transported by the cftr which doesnt work in cf could actually be replaced by the mrp2 and have it do the transport of the faulty cftr. The thought is that if you can increase mrp2 expression then you might be able to overcome some of the basic defects of CF. Their is research going on about this at the moment. One group hopes they might have found the compound to do this.
 
P

petersymons

Guest
static the thought is that what is meant to be transported by the cftr which doesnt work in cf could actually be replaced by the mrp2 and have it do the transport of the faulty cftr. The thought is that if you can increase mrp2 expression then you might be able to overcome some of the basic defects of CF. Their is research going on about this at the moment. One group hopes they might have found the compound to do this.
 
P

petersymons

Guest
static the thought is that what is meant to be transported by the cftr which doesnt work in cf could actually be replaced by the mrp2 and have it do the transport of the faulty cftr. The thought is that if you can increase mrp2 expression then you might be able to overcome some of the basic defects of CF. Their is research going on about this at the moment. One group hopes they might have found the compound to do this.
 
You must log in or register to reply here.
Top