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New article to read from @upcite.bsky.social! Increased intervals in enzyme replacement therapy for stable type 1 #Gaucher disease.

➡️ Supporting personalized spacing strategies that may improve quality of life and reduce healthcare costs.

🔗 doi.org/10.1111/joim.70079

#lysosomal #enzyme

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This image depicts a nematode with fluorescently labeled bacteria in its intestine (left), illustrating microbial metabolic input. On the right, fluorescently marked epidermal lysosomes (top), intestinal lysosomes (middle), and lipid droplets (bottom) highlight the organelles engaged in lysosome-dependent lipid degradation. Together, the image visualizes a microbiota–lysosome axis through which bacterial tryptophan metabolism reprograms host lipid homeostasis. Image Credit: Kenan Zhang

This image depicts a nematode with fluorescently labeled bacteria in its intestine (left), illustrating microbial metabolic input. On the right, fluorescently marked epidermal lysosomes (top), intestinal lysosomes (middle), and lipid droplets (bottom) highlight the organelles engaged in lysosome-dependent lipid degradation. Together, the image visualizes a microbiota–lysosome axis through which bacterial tryptophan metabolism reprograms host lipid homeostasis. Image Credit: Kenan Zhang

Microbial metabolites can influence host physiology. This study shows that #microbial production of #indole from #bacterial #tryptophan catabolism enhances #lysosomal acidification & lipase activity in nematodes & mammalian hepatocytes @plosbiology.org 🧪 plos.io/3ZZAsaI

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This image depicts a nematode with fluorescently labeled bacteria in its intestine (left), illustrating microbial metabolic input. On the right, fluorescently marked epidermal lysosomes (top), intestinal lysosomes (middle), and lipid droplets (bottom) highlight the organelles engaged in lysosome-dependent lipid degradation. Together, the image visualizes a microbiota–lysosome axis through which bacterial tryptophan metabolism reprograms host lipid homeostasis. Image Credit: Kenan Zhang

This image depicts a nematode with fluorescently labeled bacteria in its intestine (left), illustrating microbial metabolic input. On the right, fluorescently marked epidermal lysosomes (top), intestinal lysosomes (middle), and lipid droplets (bottom) highlight the organelles engaged in lysosome-dependent lipid degradation. Together, the image visualizes a microbiota–lysosome axis through which bacterial tryptophan metabolism reprograms host lipid homeostasis. Image Credit: Kenan Zhang

Microbial metabolites can influence host physiology. This study shows that #microbial production of #indole from #bacterial #tryptophan catabolism enhances #lysosomal acidification & lipase activity in nematodes & mammalian hepatocytes @plosbiology.org 🧪 plos.io/3ZZAsaI

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This image depicts a nematode with fluorescently labeled bacteria in its intestine (left), illustrating microbial metabolic input. On the right, fluorescently marked epidermal lysosomes (top), intestinal lysosomes (middle), and lipid droplets (bottom) highlight the organelles engaged in lysosome-dependent lipid degradation. Together, the image visualizes a microbiota–lysosome axis through which bacterial tryptophan metabolism reprograms host lipid homeostasis. Image Credit: Kenan Zhang

This image depicts a nematode with fluorescently labeled bacteria in its intestine (left), illustrating microbial metabolic input. On the right, fluorescently marked epidermal lysosomes (top), intestinal lysosomes (middle), and lipid droplets (bottom) highlight the organelles engaged in lysosome-dependent lipid degradation. Together, the image visualizes a microbiota–lysosome axis through which bacterial tryptophan metabolism reprograms host lipid homeostasis. Image Credit: Kenan Zhang

Microbial metabolites can influence host physiology. This study shows that #microbial production of #indole from #bacterial #tryptophan catabolism enhances #lysosomal acidification & lipase activity in nematodes & mammalian hepatocytes @plosbiology.org 🧪 plos.io/3ZZAsaI

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Two #lysosomal genes ATP13A2 and #GBA1 interact to drive #neurodegeneration

Mingxue Gu, Jinghan Zhao, Mingxi Deng...Joshua M. Shulman & Hugo J. Bellen @bcmhouston.bsky.social #Parkinsons

link.springer.com/article/10.1...

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#Lysosomal protease-mediated APP degradation is pH-dependent, mutation-sensitive, and facilitates tau #proteolysis

Caroline Ackley...Paul J. Sampognaro, Aimee W. Kao @ucsfmac.bsky.social @ucsanfrancisco.bsky.social #amyloid #AlzheimersDisease #autophagy

link.springer.com/article/10.1...

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New work from the lab of Dr. Saghi Ghaffari has shown that reversing #lysosomal dysfunction restores youthful state in aged #hematopoietic stem cells.

📘 Read it in @cp-cellstemcell.bsky.social: https://bit.ly/4pv1S2X
🎙️ Listen to the episode: https://bit.ly/4q05JW4

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'C-terminus-dependent detection of #lysosomal alpha- #synuclein in nigral #Parkinsons disease human brain neurons'

Martino L. Morella, Bana Al Khayrat, Tim E. Moors...Wilma D. J. van de Berg @amsterdamumc.bsky.social

molecularneurodegeneration.biomedcentral.com/articles/10....

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Proteome Landscapes Decode Organelle Vulnerabilities in cortical and dopaminergic-like induced neurons Across Lysosomal Storage Disorders Lysosomes maintain cellular homeostasis by degrading proteins delivered via endocytosis and autophagy and recycling building blocks for organelle biogenesis. Lysosomal Storage Disorders (LSDs) compris...

Proteome Landscapes Decode Organelle Vulnerabilities in cortical and dopaminergic-like induced neurons across #Lysosomal Storage Disorders by the Harper Lab at @harvardcellbio.bsky.social www.biorxiv.org/content/10.1...

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APP ubiquitination by VHL protein is essential for MVB sorting and lysosomal degradation Abstract. Amyloid precursor protein (APP), a type I transmembrane protein, is closely related to the pathogenesis of Alzheimer’s disease (AD). Amyloid beta

APP ubiquitination by VHL protein is essential for MVB sorting and #lysosomal degradation academic.oup.com/jmcb/advance...

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The C. elegans PVD neuron morphology in wild-type (upper) versus TFEB/hlh-30 loss-of-function mutant (lower) animals in mid-adulthood. In the TFEB/hlh-30 mutant, but not in wild-type, dendrite degeneration and disorganized outgrowths are visible.

The C. elegans PVD neuron morphology in wild-type (upper) versus TFEB/hlh-30 loss-of-function mutant (lower) animals in mid-adulthood. In the TFEB/hlh-30 mutant, but not in wild-type, dendrite degeneration and disorganized outgrowths are visible.

How do #neurons maintain adequate lysosomal function during adulthood? This study shows that basal HLH-30 activity is essential for maintaining neuronal #lysosomal function & structural integrity in #Celegans, protecting against aging-related dendritic defects @plosbiology.org 🧪 plos.io/4nU79QF

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The C. elegans PVD neuron morphology in wild-type (upper) versus TFEB/hlh-30 loss-of-function mutant (lower) animals in mid-adulthood. In the TFEB/hlh-30 mutant, but not in wild-type, dendrite degeneration and disorganized outgrowths are visible.

The C. elegans PVD neuron morphology in wild-type (upper) versus TFEB/hlh-30 loss-of-function mutant (lower) animals in mid-adulthood. In the TFEB/hlh-30 mutant, but not in wild-type, dendrite degeneration and disorganized outgrowths are visible.

How do #neurons maintain adequate lysosomal function during adulthood? This study shows that basal HLH-30 activity is essential for maintaining neuronal #lysosomal function & structural integrity in #Celegans, protecting against aging-related dendritic defects @plosbiology.org 🧪 plos.io/4nU79QF

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The C. elegans PVD neuron morphology in wild-type (upper) versus TFEB/hlh-30 loss-of-function mutant (lower) animals in mid-adulthood. In the TFEB/hlh-30 mutant, but not in wild-type, dendrite degeneration and disorganized outgrowths are visible.

The C. elegans PVD neuron morphology in wild-type (upper) versus TFEB/hlh-30 loss-of-function mutant (lower) animals in mid-adulthood. In the TFEB/hlh-30 mutant, but not in wild-type, dendrite degeneration and disorganized outgrowths are visible.

How do #neurons maintain adequate lysosomal function during adulthood? This study shows that basal HLH-30 activity is essential for maintaining neuronal #lysosomal function & structural integrity in #Celegans, protecting against aging-related dendritic defects @plosbiology.org 🧪 plos.io/4nU79QF

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Recombinant cathepsins B and L promote α-synuclein clearance and restore lysosomal function in human and murine models with α-synuclein pathology - Molecular Neurodegeneration The autophagy-lysosomal pathway is crucial for maintaining homeostasis and survival of neurons, hence defects in this system have been associated with neurodegeneration, including Parkinson's disease ...

Recombinant #cathepsins B and L promote α-synuclein clearance and restore #lysosomal function in human and murine models with α-synuclein pathology

Denise Balta, Anish Varghese, Susy Prieto Huarcaya..Friederike Zunke @fau.de #Parkinsons

molecularneurodegeneration.biomedcentral.com/articles/10....

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ATXN3-p97 facilitates #lysosomal restoration after damage by deubiquitinating LAMP2 and targeting it for degradation via microautophagy
Hemmo Meyer and coworkers @hemmo-lab.bsky.social
www.embopress.org/doi/full/10....

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Announcing the launch of our #Seed #Funding #Round as we take the next step in our mission to transform the future of #enzyme #replacement #therapies for #lysosomal #storage #diseases.

With a passionate team, early proof-of-concept data, and a clear path to the clinic, we’re ready to scale!

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Check out this article from Physiological Reviews, TPCs: FROM PLANT TO HUMAN

Yvonne Eileen Klingl, et al.
ow.ly/QgKZ50W3ZLi
#Lysosomal #TPC @lmu-klinikum.bsky.social‬

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Using GeoMx Spatial Transcriptomics on adjacent slices for rucaparib and niraparib-treated PDEs, we compared high and low drug regions. High drug regions were enriched in apoptotic signatures, and intriguingly, we also found an association with #lysosomal signatures!

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@karkam.bsky.social (#1919) presented exciting discoveries on AP-5 disease at at #ARVO2025 This is a novel Lysosomal Macular Dystrophy and also defines a new RPE disease. Great collaboration of the ERDC www.erdc.info @carlorivolta.bsky.social
#maculardystrophy #lysosomal #AP5 #RPEdisease

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I won’t attend but please get in touch with Susan and Alice if you want to know more about our #advanced #therapeutics for #lysosomal #storage #disorders.

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Increased TMEM106B levels lead to lysosomal dysfunction which affects synaptic signaling and neuronal health - Molecular Neurodegeneration Background Genetic variation in Transmembrane protein 106B (TMEM106B) is known to influence the risk and presentation in several neurodegenerative diseases and modifies healthy aging. While evidence f...

'Increased #TMEM106B levels lead to #lysosomal dysfunction which affects synaptic signaling and neuronal health'

@jolienperneel.bsky.social @mirandalastraosua.bsky.social Sara Alidadiani... Xiaolai Zhou & Rosa Rademakers @cmn-vib.bsky.social @uantwerpen.be

bit.ly/4lG76ro

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Welcome to the Stracquadanio Lab A data-driven synthetic biology lab using machine learning and synthetic biology to understand cancer biology.

Hi there! Officially starting my new academic account on @bsky.app.

My group works on generative #AI models and #hightroughput #protein #expression and #screening platforms to engineer potent therapies for #lysosomal #storage #diseases. Learn more at: www.stracquadaniolab.org

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SPIN-POV this week by Dr Prasad Hanagandi..
#Lysosomal spectrum should be high on list of differentials when one finds dark thalami on T2 sequences in a suspected case of Neurometabolic/ Neurodegenerative disorder..
#pedineurorad

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Hello everyone, happy to share my first post here on BSky. I've moved over from Twitter and looking forward to seeing and discussing interesting science here. Please give me a follow if you're interested in #Lewy body diseases or #lysosomal storage disorders.
Thank you!

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