p53 tagged posts

Newly Synthesized Fungal Compound can switch on a Self-Destruct Button for Cancer

A newly synthesized version of a fungal compound could be a powerful new tool against cancer
A newly synthesized version of a fungal compound could be a powerful new tool against cancer
vitanovski/Depositphotos

Leading organic chemists synthesize fungal molecule capable of reactivating the self-destruct gene in aggressive cancer cells. Cancers cells use a special technique to propagate; they delete their ‘programmed death’ gene through mutation, ‘forget’ to die when their lifetime is over, and continue to grow instead. A research team has developed a method through which a fungal compound capable of rearming the self-destruct gene in certain cancer cells can be artificially produced in marketable quantities, providing a potential cancer therapeutic strategy.

All human body cells have a certain lifespan, during which they perform their essential duties...

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Opposite effect: Protein widely known to Fight Tumors also Boosts Cancer Growth

UC San Diego researchers found that the PUMA protein works inside the cell’s mitochondria to switch energy production processes and stimulate cancer growth.
Credit: Xu Lab, UC San Diego

Researchers find evidence that genome ‘guardian’ can stimulate cancer. Researchers studying p53, the heralded cancer-fighting ‘guardian of the genome,’ found that the human protein also plays a role in promoting tumors, in addition to suppressing them. They found that the PUMA protein works inside the cell’s mitochondria to switch energy production processes and stimulate cancer growth. Search for a description of “p53” and it becomes clear that this human protein is widely known for its cancer-fighting benefits, leading to its renown as “the guardian of the genome.”

Scientists at the University of Ca...

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How Proteins Control Gene Expression by Binding both DNA and RNA

A model for cooperative control of the p53 pathway by Mdm2 and Mdmx. In the absence of stress signals, the primary function of Mdm2 is to maintain p53 at low levels, whereas Mdmx contributes to the overall inhibition of p53 independently of Mdm2. Mdmx inhibits p53 transcriptional activity, whereas the contribution of Mdm2 to the regulation of p53 transcriptional activity per se is still unclear and a matter of debate

A model for cooperative control of the p53 pathway by Mdm2 and Mdmx. In the absence of stress signals, the primary function of Mdm2 is to maintain p53 at low levels, whereas Mdmx contributes to the overall inhibition of p53 independently of Mdm2. Mdmx inhibits p53 transcriptional activity, whereas the contribution of Mdm2 to the regulation of p53 transcriptional activity per se is still unclear and a matter of debate

Proteins that bind DNA or RNA are usually put in different categories, but researchers at Umeå University in Sweden and Inserm in France recently showed how p53 protein has the capacity to bind both and how this controls gene expression on the levels of both transcription (RNA synthesis) and mRNA translation (protein synthesis).

The p53 tumour suppressor protein is best known...

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Brothers-in-arms: How p53 and Telomeres work together to stave off Cancer

Binding of p53 to non‐canonical response elements in human subtelomeres confers enhancer‐like activities and correlates with increased telomere stability. Non‐canonical p53 binding sites were identified in the subtelomeres of both human and mouse. Subtelomeric p53 response elements confer transcription activation in vitro and p53‐dependent induction of TERRA, eRNA‐like transcripts, and more distal subtelomeric genes. p53 status correlates with enhanced telomere stability and survival in response to etoposide‐induced DNA damage. Stress‐induced p53 binding to the subtelomere correlates with increased histone acetylation and decreased γH2AX. CRISPR deletion of the p53 response element ameliorates these effects.

Binding of p53 to non‐canonical response elements in human subtelomeres confers enhancer‐like activities and correlates with increased telomere stability. Non‐canonical p53 binding sites were identified in the subtelomeres of both human and mouse. Subtelomeric p53 response elements confer transcription activation in vitro and p53‐dependent induction of TERRA, eRNA‐like transcripts, and more distal subtelomeric genes. p53 status correlates with enhanced telomere stability and survival in response to etoposide‐induced DNA damage. Stress‐induced p53 binding to the subtelomere correlates with increased histone acetylation and decreased γH2AX. CRISPR deletion of the p53 response element ameliorates these effects.

New research shows p53 is able to suppress accumulated DNA damage a...

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