Breakthrough discoveries have increased our understanding of the mechanisms that regulate kinase activity. We bring research in this area together in our latest Special Issue: Allosteric Regulation of Kinase Activity. Read now:
eLife Sciences Publications, Ltd.’s Post
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Finding a reliable and scalable source of microglia for compound screening and #drugdevelopment is challenging. Human iPSC-derived cells could be the answer. Learn how they compare to human post-mortem microglia in #neuroinflammation assays. https://okt.to/nL9TpX
Microglia Cell Lines to Model Neuroinflammation In Vitro
criver.com
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Finding a reliable and scalable source of microglia for compound screening and #drugdevelopment is challenging. Human iPSC-derived cells could be the answer. Learn how they compare to human post-mortem microglia in #neuroinflammation assays. https://okt.to/43RlxK
Microglia Cell Lines to Model Neuroinflammation In Vitro
criver.com
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Drug Design ,Drug Discovery, Medicinal Chemistry|| Adjunct Professor || Author of Applied Organic Chemistry(Wiley), Fundamentals of Cancer Detection, Treatment, and Prevention (Wiley), Medicines for Cancer (Elsevier)
Leniolisib: a novel treatment for activated phosphoinositide-3 kinase delta syndrome https://lnkd.in/gqj7Ui5Y
Frontiers | Leniolisib: a novel treatment for activated phosphoinositide-3 kinase delta syndrome
frontiersin.org
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Finding a reliable and scalable source of microglia for compound screening and #drugdevelopment is challenging. Human iPSC-derived cells could be the answer. Learn how they compare to human post-mortem microglia in #neuroinflammation assays. https://okt.to/vL0gK6
Microglia Cell Lines to Model Neuroinflammation In Vitro
criver.com
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If you are working on #neuroinflammation #drugdevelopment you might be interested in checking this human iPSC derived microglia in vitro assays to support your research #neuroscience #neurodegeneration #microglia
Finding a reliable and scalable source of microglia for compound screening and #drugdevelopment is challenging. Human iPSC-derived cells could be the answer. Learn how they compare to human post-mortem microglia in #neuroinflammation assays. https://okt.to/vL0gK6
Microglia Cell Lines to Model Neuroinflammation In Vitro
criver.com
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Finding a reliable and scalable source of microglia for compound screening and #drugdevelopment is challenging. Human iPSC-derived cells could be the answer. Learn how they compare to human post-mortem microglia in #neuroinflammation assays. https://okt.to/2CHgDM
Microglia Cell Lines to Model Neuroinflammation In Vitro
criver.com
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Crossing the Blood Brain Barrier (#BBB) A study suggesting that in vitro models developed using data from Parallel Artificial Membrane #Permeability Assay ( #PAMPA- #BBB ) can forecast in vivo brain permeability. https://lnkd.in/eueGUg9F #drugdevelopment #drugpermeability #PAMPA #bloodbrainbarrier #BBBPAMPA
Small molecule blood brain barrier permeability prediction
pion-inc.com
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New publication by Control of local mRNA expression research group: KIS counteracts PTBP2 and regulates alternative exon usage in neurons This study provides important new insights into the regulation of alternative splicing in neurons by the kinase KIS. The results obtained demonstrates how KIS-mediated phosphorylation of the splicing regulator PTB2 controls exon usage during neuronal differentiation. Moreno-Aguilera M, Neher AM, Mendoza MB, Dodel M, Mardakheh FK, Ortiz R, Gallego C. (2024). KIS counteracts PTBP2 and regulates alternative exon usage in neurons. eLife. Apr 10;13:e96048. doi: 10.7554/eLife.96048 https://lnkd.in/dSpshf79
KIS counteracts PTBP2 and regulates alternative exon usage in neurons - IBMB - Institut de Biología Molecular de Barcelona
https://www.ibmb.csic.es
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A large host of cytokines and hormones transmit their signals via the janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway. JAKs are protein tyrosine kinases (PTKs) that mediate signal transduction downstream of cytokine receptors and display key targets for #DrugDesign of allosteric small molecule inhibitors. #cryoEM
Structural basis of Janus kinase trans-activation
cell.com
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Exciting Research Alert! Our latest co-author paper from my previous “Mehta’s lab, Department of pharmacology, College of Medicine, University of Illinois”, Chicago, explores into the intricate mechanisms governing endothelial cell behavior and its implications for acute lung injury (ALI). In this paper we've uncovered how the mechanical environment orchestrated by endothelial cells (ECs) plays a pivotal role in maintaining lung health. Specifically, our study highlights the crucial role of focal adhesion kinase (FAK) in safeguarding tension transmission to the nucleus, thus preserving the restrictive fate of ECs. By unraveling this mechanism, we shed light on how aberrant tension transmission can lead to the transition from restrictive to leaky endothelium, a hallmark of ALI. Our findings demonstrate that FAK depletion triggers a cascade of events, including heightened EC tension and altered gene expression patterns, ultimately contributing to endothelial dysfunction. Importantly, this research offers insights into potential therapeutic avenues for ALI by targeting FAK and its downstream effectors. By restoring the balance of tension transmission, we aim to mitigate endothelial dysfunction and preserve lung homeostasis. 📖 "Read our paper to learn how mechanical forces affect endothelial behavior, which could help develop new treatments for ALI." #Research #EndothelialHealth #LungHomeostasis
FAK regulates tension transmission to the nucleus and endothelial transcriptome independent of kinase activity
cell.com
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