"Following Inhibition of BCL-2 by Antisense Oligonucleotides Compensatory Suppression of Apoptosis Involves the Direct Signal Transduction Pathway of LNCaP Cells"
written by Marvin Rubenstein, Courtney M. P. Hollowell, Patrick Guinan,
published by Open Journal of Apoptosis, Vol.4 No.1, 2015
has been cited by the following article(s):
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[1] Progress in the Use of Antisense Oligonucleotides for Vaccine Improvement
2020
[2] Not All Regulators of Apoptosis are Equally Affected by Compensation Following BCL-2 Suppression by Antisense Oligonucleotides: A Review
Cancer Science & Research, 2019
[3] Mechanisms by Which Non-Targeted Genes Compensate for Specific Gene Therapy Directed Towards Bcl-2 in a Prostate Cancer Model
2017
[4] Suppression of BCL-2 by antisense oligonucleotides is compensated through increased activity of the androgen receptor, ARv7 and coactivators
2017
[5] Suppression of Bcl-2 by Antisense Oligonucleotides is Compensated through Increased Activity of the Androgen Receptor and Co-Activators but not 5-alpha Reductase
Cancer Research and Oncology: Open Access, 2016
[6] Suppression of bcl-2 by antisense oligonucleotides is compensated through increased activity of the androgen receptor and co-activators but not 5-alpha …
2016
[7] Expression of TMPSS22, Androgen Receptor and its Co-Activators are Increased Following Suppression of Bcl-2 by Antisense Oligonucleotides: But the …
2016
[8] Altered Oncogene Activity Contributes to Compensation for Antisense Suppression of Bcl-2 and Tumor Resistance
Open Journal of Apoptosis, 2015
[9] Following BCL-2 Suppression by Antisense Oligonucleotide Compensation by Non-Targeted Genes Does Not Involve TGF-β1
EC Microbiology, 2015
[10] Suppression of BCL2 by Antisense Oligonucleotides and Compensation by Non-Targeted Genes May Enhance Tumor Proliferation
In Vivo, 2015
[11] Suppression of bcl-2 by antisense oligonucleotides results in compensation and enhanced tumor proliferation involving KI-67
Symbiosis, 2015