Top Tweets for #narf
Tuesday J1 low year of the dragon, Jordan/Clot one of a kind shorts and Space Cowboys fitted. Have a great day and try to take over the world. #Narf
#HasbroStore三井アウトレットパーク滋賀竜王 店
ゴールデンウィークセール開催中です‼️
数日前に売り場を増やして新商品もたくさん出しました✨
今までにないほどセール商品が増えていて、どれもすごくお得なのでこの機会に是非ゲットしちゃってくださいね🙌🎁
#marvel #STARWARS #NARF #ファービー
Roast News Service – RNS – Thursday 16 April 2026
#AJAX #ZEN #SVML #NARF #GSCU #NTVO #MILA #GWMO #BRES #ORR #UJO
Ajax Resources Plc (AQSE: AJAX) has provided an update on the potential divestment of its Eureka Gold and Copper Project, confirming it is now in exclusive negotiations with a large Chinese mining group following positive preliminary technical due diligence, with a site visit expected imminently and discussions progressing toward potential binding terms, while also terminating the La Norteña acquisition due to vendor breach; the strategy is clearly focused on extracting value from Eureka while sharpening focus on higher-priority assets and near-term activity at Macacha.@ajax_plc
#narf #zort
We relaunched…
And…
We secured the PINKANDTHEBRAIN.SOL @SolNameService ID 🔥🔥🔥
Link:
https://t.co/79uhZJxNW1
with D’Ville Crypto Solutions @dcscrypto
#pinkyandthebrain #animaniacs
The world according to #Narf
If you understand what they did to cell membrane you can only get scared: From my planned IPAK-Presentation:
"Let me briefly summarize where we are now, because at this point we have the two most critical puzzle pieces to understand how membrane organization controls cellular signaling and why LNPs are a real issue with unknown long-term safety potential, an issue that goes far beyond modRNA and Spike Proteins.
First: PIPs, particularly PI(4,5)P2, function as electrostatic organizers of the membrane. They do not just provide substrate for second messenger production. They define where signaling can occur, which proteins can bind, and how signaling platforms assemble spatially.
Second: Signal transduction operates through threshold logic and competitive binding at these PIP-enriched membrane domains. Small perturbations in the electrostatic landscape do not simply reduce one signal. They reorganize the competitive balance across multiple pathways simultaneously.
Now we need to understand how this electrostatic organization translates into biochemical signaling cascades to provide the logic why LNPs will disturb this complete network in unpredictable manor and will change the whole cell behavior. NSP.
Slide 19
This perspective was demonstrated by Zhang and colleagues for Muscarinic-current channels, or KCMQ. We will take a closer look because this illustrates the most critical aspect of how charged lipids control signaling through hard physics. My slide summarizes three studies to provide a holistic picture of how electrostatic membrane properties translate into biochemical signaling interactions.
As Zhang and colleagues showed, if you alter the membrane charge or lipid composition, you don't just reduce signaling. You reorganize where signaling can occur. Receptors are clustered in lipid rafts, and PI(3,4,5)P3 is formed in these localized, charge-dependent regions. Any disturbance reshapes the spatial signaling landscape, and due to feedback mechanisms, small membrane-level changes propagate into large downstream effects.
But there's more. Szentpetery and colleagues demonstrated that PI(4,5)P2 accumulation at the plasma membrane recruits oxysterol-binding proteins like ORP8, which mediate phosphatidylserine-PIP2 exchange between the ER and plasma membrane. This maintains the lipid composition required for membrane organization.
And critically, as Chung and colleagues showed, PI4KIIIα drives the PI4P gradient that controls ORP5/8 function, and through that, controls KRAS localization. KRAS requires phosphatidylserine-rich domains for membrane association. If the PI4P gradient is disrupted, ORP5/8 cannot function, phosphatidylserine distribution becomes dysregulated, and KRAS dissociates or mislocalizes.
Given that even a 25% reduction in KCNQ channel function leads to epilepsy, and that Zhang showed how single amino acid mutations affecting PIP2 binding dramatically increase receptor-mediated inhibition, the system's sensitivity to electrostatic perturbation is evident. And this may become a bigger issue for LNPs than we actually notice and have noticed so far. And this is where I become emotional: We are not dealing with a system that tolerates noise. We are dealing with a precision instrument.
In other words: disrupting the PIP landscape simultaneously reorganizes lipid trafficking, spatial organization of signaling platforms, and the competitive balance of multiple pathways, including both RAS/RAF/MEK/ERK-MAPK and PI3K/AKT/mTOR-complexes. So the question is: if a system fails when there is a 25% malfunction—how many other cellular precision instruments have similarly tight tolerances, and which of them affect LNPs? NSP. "
The St. Canard Files would like to wish our favorite Steelbeaked F.O.W.L. agent, Rob Paulsen a very happy birthday.
#happybirthdayrobpaulsen #robpaulsen #steelbeak #raphael #yakkowarner #pinky #narf #carlwheezer #pjpete
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