Congratulations!!

Registration is still open, and abstracts for posters are still accepted (email me for info or questions)!

Congratulations!!

A big thank you for the GENEROUS support, although general support is good too! :)

A big Thank You to the general support from the NIH-NHLBI, the Leducq Foundation, the American Heart Association @ahascience.bsky.social, a Fleming Research Fellowship, and the Mills family.

Expression of a dominant negative nesprin domain, DN KASH, which disrupts the LINC complex, reduces forces on the nucleus, reduces nuclear envelope rupture, and restores expression of many dysregulated genes. DN KASH expression also rescues cardiac function and extends survival by >1 year.

Detailed transcriptomic analyses indicate that a subset of cardiomyocytes drives disease progression by expression of genes associated with sterile inflammation, likely downstream of nuclear envelope rupture and activation of cytosolic DNA sensors, independent of cGAS/STING.

Thanks so much for highlighting our work!

I should point out that the conference is held in Melbourne, Florida, not Australia!

Speakers include: @luskinglab.bsky.social @renkawitzteam.bsky.social @pcusachs.bsky.social @gabrielneurohr.bsky.social @simonereber.bsky.social @zierlab.bsky.social @katemiro.bsky.social @sarawickstrom.bsky.social @rashmi-priya.bsky.social @stroudlab.bsky.social @becklab.bsky.social & many more!

You are very welcome. It’s been a pleasure reading and highlighting your beautiful work and the evidence you present for how ER tubules are anchored to actin filaments and focal adhesions!

…and it provides a better understanding of the normal function of lamins, particular in skeletal and cardiac muscle cells. The work was led by the amazing Jacob Odell and supported by the National Institutes of Health (NIH), National Science Foundation (NSF), and Leducq Foundation.
.

This effect is due to the unique rod domain of lamin A/C, and does not require the lamin Ig-fold or tail, nor unique binding partners. This work has direct implications for our understanding of how mutations in the LMNA gene cause muscular dystrophy and heart disease…