HIV-1 Tat Protein Enhances Expression and Function of Breast Cancer Resistance Protein

2016 ◽  
Vol 32 (1) ◽  
pp. 1-3 ◽  
Author(s):  
Yancong Zhou ◽  
Kun Zhang ◽  
Xiaojie Yin ◽  
Qichang Nie ◽  
Yonggang Ma
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Resistance Protein ◽  
Cancer Resistance ◽  
Tat Protein ◽  
Resistance Protein ◽  
And Function ◽  
Hiv 1

scholarly journals Breast cancer resistance protein (BCRP/MXR/ABCG2) in acute myeloid leukemia: discordance between expression and function

Leukemia ◽  
2004 ◽  
Vol 18 (7) ◽  
pp. 1252-1257 ◽  
Author(s):  
A Suvannasankha ◽  
H Minderman ◽  
K L O'Loughlin ◽  
T Nakanishi ◽  
W R Greco ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Breast Cancer Resistance Protein ◽  
Cancer Resistance ◽  
Resistance Protein ◽  
And Function ◽  
Acute Myeloid

Pointer the Role of Breast Cancer Resistance Protein (BCRP/ABCG2) in Cellular Resistance to HIV-1 Nucleoside Reverse Transcriptase Inhibitors

2005 ◽  
Vol 16 (4) ◽  
pp. 213-216 ◽  
Author(s):  
Xin Wang ◽  
Masanori Baba
Keyword(s):  
Breast Cancer ◽  
Reverse Transcriptase ◽  
Breast Cancer Resistance Protein ◽  
Cancer Resistance ◽  
Reverse Transcriptase Inhibitors ◽  
Nucleoside Reverse Transcriptase Inhibitors ◽  
Cellular Resistance ◽  
Resistance Protein ◽  
Anti Hiv ◽  
Hiv 1

Treatment of HIV-1-infected patients with antiretroviral agents is not always successful due to the emergence of resistant HIV-1 mutants with reduced susceptibility to the agents. However, factors other than viral mutation may also contribute to treatment failure. It has been demonstrated that the ATP-binding cassette (ABC) transporter P-glycoprotein (P-gp/ABCB1) is a key determinant of oral bioavailability of HIV-1 protease inhibitors and their penetration of the central nervous system. More recently, we have found that the expression of breast cancer resistance protein (BCRP/ABCG2) in a CD4+ T-cell line confers cellular resistance to nucleoside reverse transcriptase inhibitors (NRTIs). The anti-HIV-1 activity of the NRTI zidovudine (AZT) was significantly diminished through the reduction of its metabolite levels in MT-4 cells which express high levels of BCRP. Moreover, the BCRP-specific inhibitor fumitremorgin C could completely restore the cytotoxicity of AZT and intracellular levels of its metabolites in BCRP-expressing cells. Thus, BCRP is considered to be a cellular factor that modulates the anti-HIV-1 activity of NRTIs.

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