Need of the hour: “The Bend it like Beckham” kind of science in India.

A conference to watch out.

Salute to Dr. Prahlada Ramarao, the nation owes you Sir.

May issue, 2025; Nature Microbiology @NatureMicrobiol.

Lung immune cells as peacekeepers against virus infiltration.

RT @iitbombay: A study by a team led by Prof. Anirban Banerjee reveals how a host protein named VCP/p97 works like an elite special operati….

Journey of @SouravSGW while discovering a brand-new facet of innate immunity against pathogens. Thank you @biopatrika for featuring this and kudos @SouravSGW, you deserve all the accolades. Hope you won’t stop here.

RT @DipaLab_IISc: Glad to share that our collaborative project is now online in Nature Microbiology. Primarily conducted by PhD student Sou….

@iitbombay @BsbeIitb @ANRFIndia @ignitelsf @India_Alliance.

An insightful description and perspective on our recent discovery on a “unique mechanical force based method adopted by host cell to kill bacteria @NatureMicrobiol .#p97 #AAAATPase #Ubiquitin #Pathogen #Cellularimmunity.

9/9 Thanks to @ANRFIndia (erstwhile SERB) and @ignitelsf for funding and @BsbeIitb @iitbombay @iiscbangalore for facilities. @India_Alliance @DBTIndia @IndiaDST @ICMRDELHI @CSIR_IND @The_MRC @EduMinOfIndia.

8/9 Thanks to stellar effort from @SouravSGW for spearheading this and ably supported by others in the lab as well as superb collaborative efforts from @Jmondal_tifrh @sandiplk @DipaLab_IISc and Prof. Roop Mallik at BSBE, IIT Bombay.

7/9 We also found that host apply this unique defence strategy against variety of pathogens, irrespective of their nature or origin an ability evolutionary inherited from our unicellular ancestors.

6/9 Using a murine sepsis model of Streptococcus pneumoniae infection, we show that p97 limits bacterial proliferation in vivo and protects the host from septic shock, highlighting its crucial role in immune defence.

5/9 Using in-vitro reconstitution, optical traps & electron microscopy, we reveal that p97 uses ATP-driven force to extract bacterial surface proteins, in turn ripping apart the pathogen, releasing their internal contents.

4/9 Our findings reveal four key criteria that dictates p97’s recruitment to bacterial surfaces: (1) Cytosolic exposure, (2) K48-polyUb modification, (3) Presence of ubiquitinable substrates, (4) Recognition by ubiquitin binding cofactors, in this case NPLOC4-UFD1.

3/9 We discovered that host cell unleashes a tweezer-like nanomachine, 🔥VCP/p97🔥, which plucks out these ubiquitinated proteins from bacterial surfaces to disintegrate them and halt infection at its core.

2/9 To tackle the threat, cells tag the surface proteins of these microbes with a death signal: 🚩#Ubiquitin, which marks them for destruction (. But what happens after a pathogen is tagged with ubiquitin?

1/9 We are exposed to countless pathogens every now and then but rarely fall sick. Thanks to our immune system which efficiently disposes them, keeping us safe. But pathogens continuously attack and invade the host cell’s cytosol to gain nutrients and proliferate.

🚨“Ripping bacteria to shreds” 🚨 VCP/p97, a cellular AAA-ATPase, targets and then using its tweezer like action rips apart bacteria, protecting us from infections. A thread 🦠💥#MolecularMachines #HostDefense #cellularimmunity #microbiology.@NatureMicrobiol