Sentences with phrase «activates tumor suppressor»

A new study led by University of Kentucky researchers suggests that activating the tumor suppressor p53 in normal cells causes them to secrete Par - 4, another potent tumor suppressor protein that induces cell death in cancer cells.

Not exact matches

They propose that normal tissue becomes primed for cancer when oncogenes are activated and tumor suppressor genes are silenced or lost, but that cancer develops only when a cell in the tissue reverts to a more primitive, embryonic state and starts dividing.

Declining ATP levels activate a cellular energy sensor AMPK, which adds a phosphate group to tumor suppressor protein p53, extending the protein's lifetime.

Poor repair of these «double - strand breaks» can activate cancer - causing genes or inactivate tumor - suppressor genes.

In humans, cancer develops when genes that suppress cancer, known as tumor suppressors, are lost and when mutations or genes that promote cancer, known as oncogenes, are gained or activated.

In fact, KLF4 blocks senescence and apoptosis by repressing transcription of P53, whereas it can activate P21 - dependent cell - cycle arrest, and therefore, KLF4 can function both as a tumor suppressor and an oncogene (33, 34).

It has been known for a number of years that PREX2 is a GTP / GDP exchange factor that inhibits a tumor suppressor protein called PTEN, and that this process can promote tumorigenesis by activating the PI3K signaling pathway (Fine et al., 2009; Hodakoski et al., 2014; Figure 1A).

Mice that are unable to fully activate the powerful tumor suppressor p53 are resistant to high doses of radiation.

Blood clots, often in the legs, are a frequent occurrence in patients fighting glioblastoma, the most common and the most aggressive form of brain cancer. Zerrouqi and http://www.gooakley.com/ Van Meir show that a tumor suppressor gene (p14ARF) that is often mutated in glioblastoma stops them from activating blood clotting.

Preferential glycolysis has been associated with activated oncogenes and loss of tumor suppressors, both of which confer other hallmark capabilities on cancer cells.

LKB1, originally identified as a tumor suppressor protein, is currently thought as a critical regulator of cellular metabolism and growth by controlling the activity of AMP - activated protein kinase (AMPK) and also 12 other kinases that are closely related to AMPK.

Researchers have identified a protein that activates the well - known tumor suppressor gene p53 to prevent the division of cells that have damaged DNA.

In response to cellular stress such as DNA damage, oncogene activation, transcriptional inhibition, and hypoxia, tumor suppressor p53 is activated and expressed, and acts as a transcription factor to induce its target genes [1], thereby playing a central role in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4].

For example, the well known PTEN tumor suppressor gene blocks PI3K / Akt thus activating autophagy.