Decreased Expression of Multidrug Resistance-Associated Protein 4 (MRP4/ABCC4) Leads to Reduced Glucuronidation of Flavonoids in UGT1A1-Overexpressing HeLa Cells: The Role of Futile Recycling

2015 ◽  
Vol 63 (26) ◽  
pp. 6001-6008 ◽  
Author(s):  
Hua Sun ◽  
Xiaotong Zhou ◽  
Xingwang Zhang ◽  
Baojian Wu
Gene ◽  
2021 ◽  
Vol 771 ◽  
pp. 145370
Author(s):  
Prajitha Mohandas Edathara ◽  
Shivakanth Chintalapally ◽  
Venkata Krishna Kanth Makani ◽  
Chitrakshi Pant ◽  
Suresh Yerramsetty ◽  
...  

2001 ◽  
Vol 24 (9) ◽  
pp. 1032-1036 ◽  
Author(s):  
Nami IIDA ◽  
Kohji TAKARA ◽  
Nobuko OHMOTO ◽  
Tsutomu NAKAMURA ◽  
Takashi KIMURA ◽  
...  

Pharmacology ◽  
2011 ◽  
Vol 87 (3-4) ◽  
pp. 224-231 ◽  
Author(s):  
Youngjun Seo ◽  
Mihee Kim ◽  
Minjoung Choi ◽  
Sunhee Kim ◽  
Kidae Park ◽  
...  

FEBS Letters ◽  
2006 ◽  
Vol 580 (14) ◽  
pp. 3375-3380 ◽  
Author(s):  
Shingo Yasuda ◽  
Hiroyuki Taniguchi ◽  
Fabian Oceguera-Yanez ◽  
Yoshikazu Ando ◽  
Sadanori Watanabe ◽  
...  
Keyword(s):  

2004 ◽  
Vol 238 (1) ◽  
pp. 267-272 ◽  
Author(s):  
Anne Olliver ◽  
Michel Vallé ◽  
Elisabeth Chaslus-Dancla ◽  
Axel Cloeckaert

1996 ◽  
Vol 109 (7) ◽  
pp. 1975-1989 ◽  
Author(s):  
T. Nilsson ◽  
C. Rabouille ◽  
N. Hui ◽  
R. Watson ◽  
G. Warren

Using a series of chimeric and truncated N-acetylglucosaminyltransferase I (NAGT I) molecules we have shown that part of the lumenal stalk region is both necessary and sufficient for kin recognition of mannosidase II and retention in the Golgi stack. The membrane-spanning domain was not required for retention, but replacing part or all of this domain with leucine residues did have a dramatic effect on Golgi morphology. In stable cell lines, stacked cisternae were replaced by tubulo-vesicular clusters containing the mutated NAGT I. The loss of stacked cisternae was proportional to the number of leucines used to replace the membrane-spanning domain.


2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Carolina Soekmadji ◽  
Colleen C. Nelson

Emerging evidence has shown that the extracellular vesicles (EVs) regulate various biological processes and can control cell proliferation and survival, as well as being involved in normal cell development and diseases such as cancers. In cancer treatment, development of acquired drug resistance phenotype is a serious issue. Recently it has been shown that the presence of multidrug resistance proteins such as Pgp-1 and enrichment of the lipid ceramide in EVs could have a role in mediating drug resistance. EVs could also mediate multidrug resistance through uptake of drugs in vesicles and thus limit the bioavailability of drugs to treat cancer cells. In this review, we discussed the emerging evidence of the role EVs play in mediating drug resistance in cancers and in particular the role of EVs mediating drug resistance in advanced prostate cancer. The role of EV-associated multidrug resistance proteins, miRNA, mRNA, and lipid as well as the potential interaction(s) among these factors was probed. Lastly, we provide an overview of the current available treatments for advanced prostate cancer, considering where EVs may mediate the development of resistance against these drugs.


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