My next couple weeks & p53

In one of my earlier posts “Adios to this bench” & Vaccines, I mentioned that i just recently finished my first lab rotation and have a couple weeks before i start my next one in the states. The next couple weeks i have ‘off’ but will spend most of these writing my lab report on my last lab rotation, packing, and sorting some last aspects of my Visa out. Currently, I’m sat at one of my favorite cafes in the city and try to evaluate all the data I’ve collected over the past two months & prepare a bit for my next lab.


In honor of my first lab rotation, where i worked on the interaction of chaperones (proteins involved in quality control of other proteins) with a protein called ‘p53’ i will write a bit about it here.

p53 is a tumor suppressor protein, which means it makes sure that mutated or unhealthy cells do not divide, preventing tumor and ultimately cancer formation. It does this by monitoring how healthy a cell is, and can in response regulate cell repair, replication, and even induce suicide (apoptosis). For that reason, it is also called ‘guardian of the genome’.

One can imagine it like a futuristic kingdom, where the king rules. This king is a robot called robot53, a uniquely qualified multitasking robot. As long as the original software is intact, robotp53 can die and be replaced without problems. This original software is in our case, our DNA coding for p53. When the software however is infected with a virus, the fundamental instructions to put robot53 together, are corrupted. Same with our DNA – if we have a mutation in the DNA sequence coding for p53, it can lead to production of unfunctional p53. Because this robot53 is so uniquely qualified, no one can take over its role and the whole kingdom (in our case, our cell) goes bonkers, if it doesn’t do its job correctly.

A relevant thing to mention here, is that important protein- coding genes often can be compensated for by other genes (if one isn’t functional) by having overlapping functions. P53 is the exception here – the Achilles heel of evolution, because it is the sole guardian of our genome.

As a result of this, in more that 50% of human cancers p53 is mutated, because it’s soo beneficial for unregulated cell growth and cancer formation, and is therefore a substantial focus in cancer research.

Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out /  Change )

Google photo

You are commenting using your Google account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s

%d bloggers like this:
search previous next tag category expand menu location phone mail time cart zoom edit close