
Stainier Lab
@StainierLab
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Our lab studies #development #regeneration #geneticrobustness @mpi_hlr. The account is run by various lab members.
Bad Nauheim
Joined March 2022
Congratulations to Samuel Capon and coauthors on their latest study that dives into the fascinating world of phenotypic variation in Fibronectin mutants, exploring why the exact same mutation leads to different viability during embryonic development ! ๐ฅณ๐
journals.plos.org
Author summary Recent studies have identified apparently healthy individuals with mutations that would be expected to lead to disease. Why these individuals are disease resistant is not understood....
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Congratulations to the team! ๐.
Huge thanks to @ACHSEeV, the Kรถhler Foundation, and our brilliant team @StainierLab @MPI_HLR. Science is a team effort, and this award recognizes that shared dedication. More here ๐ #RareDisease #EvaLuiseKรถhler #Duchenne #DMD #TranscriptionalAdaptation.
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RT @paolo_panza: Grateful for the chance to talk with Janet Rossant and @MingxiaGu ! In this @stemcellreports podcast episode we touch on tโฆ.
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Congratulations to @TJ_ThomasJuan and all the coauthors! ๐.
Very proud to share my latest research on a novel biotechnological tool: The first use of a self-cleaving ribozyme to knock down an endogenous gene in a vertebrate model. Thanks to the @StainierLab and to my co-authors #PLOSGenetics:
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Paper alert! Congrats to Lara, @CMDooley77, @DouglasAdamoski and @TJ_ThomasJuan for their great work on identifying the first example of Transcriptional Adaption in humans!๐.
5/5 ๐ Why It Matters:.First evidence of TA in humans! This work rethinks DMD treatment, showing mRNA decay itself can drive genetic compensation. Kudos to 1st Lara! @DouglasAdamoski @TJ_ThomasJuan & team! @MPI_HLR ๐ #RareDisease.
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Well done! ๐.
Excited to share this article, where we highlight the possibility that dysregulation of genes via transcriptional adaptation, an mRNA feedback loop, may play a role in some dominant diseases. @StainierLab . A new hypothesis to explain disease dominance
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RT @marco_tarasco: PhD Position Alert: Are you interested in studying cardiac fibrosis using the zebrafish as a model? We are looking for aโฆ.
mpg.de
Job offers of the Max Planck Society and Institutes. You can combine the "jobtype" with either "research subjects" or "region". Confirm your choice with OK.
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Paper alert! ๐ฅณ.Congratulations to @Yanli_Xu_ and all coauthors for their fantastic work on the effectors of HAND2 during early cardiac development. ๐.
Thrilled to share my PhD work published in @NatureCVR ! This journey was challenging, but persistence and dedication truly paid off. A huge thank you to all my co-authors for their support, and especially to my supervisor, Didier Stainier (@StainierLab ), for his guidance!.
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Congratulations to all the authors! ๐.
flt1 inactivation promotes zebrafish cardiac regeneration by enhancing endothelial activity and limiting the fibrotic response. Read this #OpenAccess Research Article by Zhen-Yu Wang, @rmarinjuez and colleagues:.
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RT @marco_tarasco: ๐ขBIG NEWS! I am thrilled to announce that Novo Nordisk Foundation has awarded us a grant for a 4-year collaboration betwโฆ.
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RT @YHCarolYang: The Yang lab will be expanding with MRC & Wellcome funding support! Watch out for recuitment adverts for technician, postdโฆ.
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RT @PinelopiGoum: Excited to see our paper @StainierLab "The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneraโฆ.
nature.com
Nature Cardiovascular Research - The endocardium is activated immediately after injury and promotes cardiac muscle regeneration by producing growth factors. Research now shows that innate immune...
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Congratulations to @radha_kul for a fantastic presentation on epicardial-myocardial interactions during early cardiac development! Well done๐๐ฅณ.#ICDAR2024.
Grateful to all ICDAR 2024 organizers for giving me this great opportunity to present my work! ๐.Also a big shoutout to @StainierLab members for their constant support!
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Great talk by @rupal_gehlot at the ICDAR 2024 meeting on the role of hand2 in cardiac valve formation!๐๐
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