Timesh Pillay
@timeshpillay.bsky.social
34 followers 52 following 15 posts
Respiratory doctor interested in its full breadth, from molecular host-pathogen interaction to universal healthcare. Free Palestine.
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Reposted by Timesh Pillay
nickdearden.bsky.social
Amid a genocide, Starmer is sending diplomats to discuss a new trade deal with Israel. Britain is telling this genocidal government ‘one of the reasons to come to Israel is to demonstrate very strong support from the UK’

It’s revolting. We need sanctions not more trade. 1/2
Reposted by Timesh Pillay
adambienkov.bsky.social
Nigel Farage still insisting that he has "never ever, ever suggested anything other than the NHS should be free".

Here's what he's said in the past behind closed doors
timeshpillay.bsky.social
Glad someone is systematically assessing this
declassifieduk.org
We researched the BBC’s online coverage of 16 aspects of UK policy towards Israel and the pro-Israel lobby.

The BBC is covering up how Britain backs Israel, and its complicity in genocide👇
www.declassifieduk.org/national-sca...
‘National scandal’: The BBC’s Gaza cover-up
Britain’s ‘public service broadcaster’ is keeping the public in the dark about UK support for Israel’s assault on Gaza, new research finds.
www.declassifieduk.org
Reposted by Timesh Pillay
joanneflynn19.bsky.social
Tuberculosis is not going away. If the cutting edge research goes away, #TB will rage on. Harvard is being targeted including the TB Immunology contract and that trickles down to all of us working on these studies. Progress will be halted. And TB will flourish. www.bostonglobe.com/2025/04/08/m...
‘This looks bad.’ A Harvard infectious disease researcher is targeted in Trump’s review. - The Boston Globe
Sarah Fortune’s tuberculosis research was the number one project on a list of threatened funding.
www.bostonglobe.com
Reposted by Timesh Pillay
Reposted by Timesh Pillay
joanneflynn19.bsky.social
I too have been dismissed from NIAID Board of Scientific Counselors along with 3 other women and a non-white man
needhibhalla.bsky.social
Just received the email that my recent appointment to a BSC, which was supposed to be until June 2029, was terminated effective immediately.
scott-delaney.bsky.social
More political meddling at NIH:

I'm told that multiple (2-4ish) members of the Boards of Scientific Counselors, which oversee intramural research, have been kicked off the boards before their term expires.

No explanation given, but the thought is that these were folks who cared about DEI.
timeshpillay.bsky.social
It was a team effort! I’m lucky to have worked with and learnt from knowledgeable, experienced and inspiring supervisors & co-authors, and many more in the Crick and Imperial infection communities. I look forward to the discussions and further study that come from this work 🦠
timeshpillay.bsky.social
For this and much much more read the full paper, now available on biorxiv biorxiv.org/content/10.1... 9/11
biorxiv.org
timeshpillay.bsky.social
In infection, SteC without its C-tail was translocated into the host cell just like wild-type, but failed to localise to the tip of the Salmonella and was unable to polymerise actin. This suggests the C-tail localises SteC for efficient kinase activity in the host cell. 8/11
timeshpillay.bsky.social
Meanwhile the C-tail of SteC, which is predicted to be poorly structured, is dispensable for SteC activity in vitro and is not required for actin polymerisation in transfected human cells. So what is the role of the C-tail? 7/11
timeshpillay.bsky.social
Furthermore, Salmonella infected into human cells requires phosphorylation of SteC at S379 for its functions to be seen. 6/11
timeshpillay.bsky.social
To our surprise, we found that SteC is activated through phosphorylation by a host kinase at serine 379. Without this, SteC is less able to phosphorylate its known substrates in vitro, and is unable to polymerise actin in human cells transfected with the steC gene. 5/11
timeshpillay.bsky.social
AlphaFold2 predicts the structure of SteC to contain a minimal kinase domain, lacking key expected features compared to known kinases, and containing a poorly structured C-tail. Despite this, SteC still functions as a kinase. How? 4/11
timeshpillay.bsky.social
So what better enzyme to study than SteC, a kinase found in pathogenic strains of Salmonella? Once Salmonella enters the host cell, it translocates SteC into the host cytoplasm via its type 3 secretion system, where it phosphorylates host proteins leading to actin polymerisation. 3/11
timeshpillay.bsky.social
Kinases, arguably the best studied enzyme class, add phosphate onto target proteins, usually at serine, threonine or tyrosine residues. This process is called phosphorylation. 2/11
timeshpillay.bsky.social
During my PhD at @crick.ac.uk and @imperialcollegeldn.bsky.social, I explored the molecular interaction between host and pathogen. My question: How have pathogenic bacteria evolved to manipulate their host environment during infection? 🦠https://biorxiv.org/content/10.1101/2025.03.01.640964v1 1/11