Incredibly grateful to receive the Gunter Blobel Early Career Award. Thank you ⁦@ASCBiology⁩ for this recognition. Congratulations to all awardees incl. my former mentor Pietro De Camilli ⁦@PDClab⁩ who received the EB Wilson Medal ! 🍾🍾🙏

Thanks to @DannieEngle @MaraShermanLab @Joshilabyale & Diana Hargreaves for organizing an amazing meeting ! #MechModels2025 @salkinstitute

RT @Aiims1742: New @iScience_CP paper by @NinaSteele17 @Pasca_Lab .Primary and metastatic cellular landscapes in human #PancreaticCancer .h….

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RT @MartinUCSF: Tenure-track faculty search of the @Ucsf_Biochem Department is open for applications! . We are looking for creative, innov….

RT @longlabstanford: Grateful to Joan and Sandy Weill for their visionary gift, bringing the best from @Stanford @UCSF together to transfor….

More on the Weill Cancer Hub West in the SF Chronicle 👇.

Launched today- the Weill Cancer Hub West -supporting transformative cancer research collaborations btw @UCSF & @Stanford. Honored to co-lead, with @longlabstanford, our team who will study the impact of diet on pancreatic cancer initiation, progression and therapy response.

RT @NatureSMB: New online! A heterotrimeric protein complex assembles the metazoan V-ATPase upon dissipation of proton gradients https://t.….

RT @NatureSMB: New online! V-ATPase assembly at leaky lysosomes

Thank you @ZouYilong and Charles David for this thoughtful commentary on our recent study connecting PCSK9 status with PDAC metastatic tropism.

Promoted ! 🙌

RT @dvir_a: Between alarms and sheltering, I learned last night that my postdoc mentor, Professor Atul Butte @atulbutte, has passed away, a….

RT @OlzmannLab: Happy to have contributed in a small way to this very cool study from Jim Wells lab, led by Fangzhu Zhao. They developed lo….

RT @RobertoZoncu: Big congrats to grad students Claire Goul @clairegoul and Julian Yano @JulianYano on earning their PhDs from @berkeleyMCB….

@GillesRademaker 🙌

We are grateful to the granting agencies, including @AACR, NIH, The Ed Mara Passion to Win Fund and the Belgian American Education Foundation (to G.R), which supported this work.

Thank you to our wonderful collaborators and their lab members - @RobertoZoncu @YehlabUNC Eric Collisson, the German PDAC consortium, Mark Looney, Bruce Wang, Grace Kim, Kwun Wen - and to @Nature and the reviewers for their thoughtful review of our study.

These findings show that chol. uptake favors liver growth, while synthesis supports lung growth. Accordingly, PCSK9 o/e shifted liver-avid cells to the lung, while PCSK9 KO redirected lung-avid cells to the liver, establishing PCSK9 as a key regulator of metastatic organ choice.

Reliance on de novo cholesterol synthesis, enables lung-avid cells to produce intermediates like 7-dehydrocholesterol that confer resistance to oxidative stress (eg, ferroptosis) in the oxygen-rich lung environment.

The ability to uptake cholesterol and route it to the lysosome, enables liver-avid cells to maintain high mTORC1 signaling and produce an oxysterol (eg, 24-hydroxycholesterol) that can activate adjacent hepatocytes to support tumor growth.

PCSK9 is a negative regulator of LDLR - the receptor for uptake of LDL-cholesterol. Accordingly, lung-avid lines which express high PCSK9 cannot uptake LDL and instead biosynthesize cholesterol, while liver-avid lines which express low PCSK9 efficiently uptake LDL-cholesterol.