@ColinNicholsLab

Posting from Colin Nichols' electrophysiology lab at @WUSTL. Focused on ion channels biophysics & role in physiology and pathology.

 Saint Louis, Missouri
nicholslab.wustl.edu/
Joined March 2023
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  • Following524
  • Followers402
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Follow us on @bluesky ! bsky.app/profile/colinnichol…
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Colin Nichols Lab @colinnicholslab.bsky.social retweeted
Harraz Lab@Harraz_Lab26 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.… A 🧵 1/n

Control of neurovascular coupling by ATP-sensitive potassium channels - Ryan M Bowen, Nathaniel W...

Regional blood flow within the brain is tightly coupled to regional neuronal activity, a process known as neurovascular coupling (NVC). In this study, we demons...

journals.sagepub.com
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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… A 🧵 1/n

Loss of β-Cell KATP Reduces Ca2+ Sensitivity of Insulin Secretion and Trpm5 Expression

Loss-of-function mutations in ATP-sensitive potassium (KATP) channels cause hyperexcitability and insulin hypersecretion, resulting in congenital hyperinsu

diabetesjournals.org
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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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Today!
Colin Nichols Lab @colinnicholslab.bsky.social@ColinNicholsLab13 Dec 2024
Next Monday, join us for a new exciting CIMED seminar! @RohacsTibor @WUSTL
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Next Monday, join us for a new exciting CIMED seminar! @RohacsTibor @WUSTL
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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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Cell bio department retreat! @MariaSRemedi
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Excellent thesis defense by Dr. Gao! Congratulations Jian, we are very proud of you! 🥳
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Join us today for a new exciting CIMED seminar! @SlavBagria @WUSTL
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Colin Nichols Lab @colinnicholslab.bsky.social retweeted
WashU Medicine Endocrinology@WashUMedEndo3 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

Lodhi, Millman, Remedi and Silverstein achieve full professorship 

Congratulations to Irfan Lodhi, PhD; Jeffrey R. Millman, PhD; Maria S. Remedi, PhD; and Julie M. Silverstein, MD of Washington University’s Division of Endocrinology, Metabolism and Lipid Research …

endocrinology.wustl.edu
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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/… A 🧵 1/n

A novel ABCC9 variant in a Greek family with Cantu syndrome affecting multiple generations highli...

Cantu syndrome (CS) (OMIM #239850) is an autosomal dominant multiorgan system condition, associated with a characteristic facial phenotype, hypertrichosis, and multiple cardiovascular complications....

onlinelibrary.wiley.com
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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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