Key Spec Table
|Species Reactivity||Key Applications||Host||Format||Antibody Type|
|Safety Information according to GHS|
|Storage and Shipping Information|
|Storage Conditions||Maintain at 2-8°C for up 12 months from date of receipt.|
|Material Size||100 µg|
|Mouse Anti-MDR1 (P-glycoprotein) UIC2 Monoclonal Antibody - 2025983||2025983|
|Mouse Anti-MDR1 (P-glycoprotein) UIC2 Monoclonal Antibody - 2191961||2191961|
|Mouse Anti-MDR1 (P-glycoprotein) UIC2 Monoclonal Antibody - 2341086||2341086|
|Reference overview||Pub Med ID|
|Human Liver Stem Cell-Derived Microvesicles Inhibit Hepatoma Growth in SCID Mice by Delivering Antitumor MicroRNAs. |
Valentina Fonsato,Federica Collino,Maria Beatriz Herrera,Claudia Cavallari,Maria Chiara Deregibus,Barbara Cisterna,Stefania Bruno,Renato Romagnoli,Mauro Salizzoni,Ciro Tetta,Giovanni Camussi
Stem cells (Dayton, Ohio) 30 2012
Microvesicles (MVs) play a pivotal role in cell-to-cell communication. Recent studies demonstrated that MVs may transfer genetic information between cells. Here, we show that MVs derived from human adult liver stem cells (HLSC) may reprogram in vitro HepG2 hepatoma and primary hepatocellular carcinoma cells by inhibiting their growth and survival. In vivo intratumor administration of MVs induced regression of ectopic tumors developed in SCID mice. We suggest that the mechanism of action is related to the delivery of microRNAs (miRNAs) from HLSC-derived MVs (MV-HLSC) to tumor cells on the basis of the following evidence: (a) the rapid, CD29-mediated internalization of MV-HLSC in HepG2 and the inhibition of tumor cell growth after MV uptake; (b) the transfer by MV-HLSC of miRNAs with potential antitumor activity that was downregulated in HepG2 cells with respect to normal hepatocytes; (c) the abrogation of the MV-HLSC antitumor effect after MV pretreatment with RNase or generation of MVs depleted of miRNAs; (d) the relevance of selected miRNAs was proven by transfecting HepG2 with miRNA mimics. The antitumor effect of MV-HLSC was also observed in tumors other than liver such as lymphoblastoma and glioblastoma. These results suggest that the delivery of selected miRNAs by MVs derived from stem cells may inhibit tumor growth and stimulate apoptosis. Stem Cells2012;30:1985-1998.
|Activity of the Bcl-2 family inhibitor ABT-263 in a panel of small cell lung cancer xenograft models. |
Alex R Shoemaker,Michael J Mitten,Jessica Adickes,Scott Ackler,Marion Refici,Debra Ferguson,Anatol Oleksijew,Jacqueline M O'Connor,Baole Wang,David J Frost,Joy Bauch,Kennan Marsh,Steven K Tahir,Xiufen Yang,Christin Tse,Stephen W Fesik,Saul H Rosenberg,Steven W Elmore
Clinical cancer research : an official journal of the American Association for Cancer Research 14 2008
The purpose of this study was to characterize the activity of the Bcl-2 protein family inhibitor ABT-263 in a panel of small cell lung cancer (SCLC) xenograft models.
|Levels of multidrug resistance (MDR1) P-glycoprotein expression by human breast cancer correlate with in vitro resistance to taxol and doxorubicin. |
Mechetner, E, et al.
Clin. Cancer Res., 4: 389-98 (1998) 1998
To determine whether multidrug resistance (MDR1) P-glycoprotein (Pgp) expression correlated with clinical MDR1-related drug resistance, we established a protocol for quantitative measurement of Pgp expression and in vitro drug resistance in doxorubicin resistant MCF7 breast cancer cell lines and 359 freshly resected specimens of breast carcinoma. Pgp expression was detected with 4E3, UIC2, and JSB-1 monoclonal antibodies using flow cytometry and immunohistochemistry (IHC). Pgp function was determined using PSC833 in a drug resistance-reversal assay and with a three-dimensional agarose-based extreme drug resistance assay. MCF7 calibrator cell lines expressed Pgp, which was functional and in proportion to the degree of drug resistance. Flow cytometry, UIC2 shift assays, IHC scores, and determination of absorbance products by image analysis were all highly correlated (r > 0.9). Overall Pgp expression increased from 11% in untreated patients to 30% in patients who had previously received chemotherapy. Compared with Pgp-negative tumors, a significant increase in doxorubicin and Taxol resistance was seen for breast cancers that expressed Pgp, regardless of prior treatment. A strong correlation between the degree of Pgp expression and in vitro resistance to Taxol and doxorubicin (but not to 5-fluorouracil) was found when either IHC scores or image analysis-based methods were used to quantify Pgp expression (n = 185, P < 0.0001). The degree of Pgp expression strongly correlated with the degree of drug resistance in the clinical specimens studied. These data suggest that (a) Pgp contributes to clinical MDR1-related drug resistance, and (b) both intrinsic and acquired expression of Pgp in breast cancer may contribute in part to therapeutic failure and relapse.
|Anti-MDR1, conformational extracellular epitope, clone UIC2 - Data Sheet|