Posting from Colin Nichols' electrophysiology lab at @WUSTL. Focused on ion channels biophysics & role in physiology and pathology.
Joined March 2023
- Tweets 122
- Following 526
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40 Photos and videos
Colin Nichols Lab @colinnicholslab.bsky.social retweeted
26 Jan 2025
Mitochondrial Ca2 -coupled generation of reactive oxygen species, peroxynitrite formation, and endothelial dysfunction in Cantú syndrome
@vesselman @ColinNicholsLab @JCI_insight insight.jci.org/articles/vie…
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Check out our new publication "Control of neurovascular coupling by ATP-sensitive potassium channels" @Nyorkster91 @SageJournals
journals.sagepub.com/doi/10.…
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We reveal the dramatic effects of either increasing or decreasing SUR2/Kir6.1-dependent KATP activity on NVC, whether pharmacologically or genetically induced. 3/n
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The study has important implications both for monogenic KATP channel diseases and for more common brain pathologies. 4/n
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Join us today for a new exciting CIMED seminar! @zubcevic_lejla @WUSTL
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Check out our new publication "Loss of β-cell KATP reduces Ca2 sensitivity of insulin secretion and Trpm5 expression" @Nyorkster91 @ADA_Pubs
diabetesjournals.org/diabete…
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In this study we examine this phenomenon, demonstrating that the lack of insulin secretion is the result of an apparent reduced sensitivity to Ca2 . 3/n
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We show that insulin secretion can be restored when intracellular Ca2 is artificially elevated by increasing extracellular Ca2 . 4/n
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Join us today for a new exciting CIMED seminar! @WUSTL
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Join us today for a new exciting CIMED seminar! @WUSTL
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Excellent thesis defense by Dr. Gao! Congratulations Jian, we are very proud of you! 🥳
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Colin Nichols Lab @colinnicholslab.bsky.social retweeted
3 Sep 2024
Congratulations to Drs. Irfan Lodhi, Jeffrey Millman, Maria Remedi, and Julie Silverstein on achieving full professorship in their careers! Learn about each of their journeys: bit.ly/3Xs4FyM. @JeffreyRMillman @LodhiLab @WUDeptMedicine
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Check out our new publication
"A novel ABCC9 variant in a Greek family with Cantu syndrome affecting multiple generations highlights the functional role of the SUR2B NBD1" onlinelibrary.wiley.com/doi/…
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Functional assays reveal that KATP channels containing this mutation exhibit reduced sensitivity to inhibitory ATP compared to WT, providing a molecular explanation of the condition. 3/n
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The specific location of the variant also reveals an unrecognized functional role of the first glycine in the signature motif of the nucleotide binding domains in NBD1 of SUR2 subunits. 4/n
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