3 results match your criteria: "The Walter and Eliza Hall Institute (WEHI)[Affiliation]"

Investigating how transcription factors control complex cellular processes requires tools that enable responses to be visualised at the single-cell level and their cell fate to be followed over time. For example, the tumour suppressor p53 (also called TP53 in humans and TRP53 in mice) can initiate diverse cellular responses by transcriptional activation of its target genes: Puma to induce apoptotic cell death and p21 to induce cell cycle arrest/cell senescence. However, it is not known how these processes are regulated and initiated in different cell types.

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Article Synopsis
  • Mutations in the TP53 tumor suppressor gene are linked to cancer and poor responses to chemotherapy, often thought to be due to loss-of-function, dominant-negative effects, or gain-of-function activities.
  • A study using CRISPR/Cas9 showed that eliminating various TP53 mutants did not change the growth or response to treatment of several cancer cell lines and organoids, suggesting that the gain-of-function effects may not be significant.
  • The findings indicate that loss-of-function effects of TP53 are critical for tumor growth, while targeting mutant TP53 for its gain-of-function activities may not be an effective cancer treatment strategy.
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The study and application of human pluripotent stem cells (hPSCs) will be enhanced by the availability of well-characterized monoclonal antibodies (mAbs) detecting cell-surface epitopes. Here, we report generation of seven new mAbs that detect cell surface proteins present on live and fixed human ES cells (hESCs) and human iPS cells (hiPSCs), confirming our previous prediction that these proteins were present on the cell surface of hPSCs. The mAbs all show a high correlation with POU5F1 (OCT4) expression and other hPSC surface markers (TRA-160 and SSEA-4) in hPSC cultures and detect rare OCT4 positive cells in differentiated cell cultures.

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