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September 2, 2024Open Access

Supplement Figure 1 from MYBL2 Drives Prostate Cancer Plasticity: Inhibiting Its Transcriptional Target CDK2 for RB1-Deficient Neuroendocrine Prostate Cancer

Beatriz German Sarah Abou Alaiwi Kun-Lin Ho Jagpreet S. Nanda Marcos A. Fonseca Deborah L. Burkhart Anjali V. Sheahan Hannah E. Bergom Katherine L. Morel Himisha Beltran Justin H. Hwang Matthew L. Freedman Kate Lawrenson Leigh Ellis

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Abstract

A. Full membrane following CRISPR targeting of Mybl2 indicating specific targeting of our target gene. B. DKO-Ctl and DKO-Mybl2 KO cells were cultured as 2-dimensional monolayers and overall cell growth was determined by CellTiter-Glo luminescent cell viability assay.

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Cite This Study

German et al. (2024) studied this question.

synapsesocial.com/papers/68e59a30b6db64358753546c https://doi.org/10.1158/2767-9764.26898208.v1

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Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

1Supplement Figure 1 from MYBL2 Drives Prostate Cancer Plasticity: Inhibiting Its Transcriptional Target CDK2 for RB1-Deficient Neuroendocrine Prostate Cancer2024
2Table S3 from MYBL2 Drives Prostate Cancer Plasticity: Inhibiting Its Transcriptional Target CDK2 for RB1-Deficient Neuroendocrine Prostate Cancer2024
3Figure 3 from MYBL2 Drives Prostate Cancer Plasticity: Inhibiting Its Transcriptional Target CDK2 for RB1-Deficient Neuroendocrine Prostate Cancer2024
4Supplement Figure 2 from MYBL2 Drives Prostate Cancer Plasticity: Inhibiting Its Transcriptional Target CDK2 for RB1-Deficient Neuroendocrine Prostate Cancer2024
5Supplement Figure 2 from MYBL2 Drives Prostate Cancer Plasticity: Inhibiting Its Transcriptional Target CDK2 for RB1-Deficient Neuroendocrine Prostate Cancer2024