Taufiq Rahman

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Taufiq Rahman

Taufiq Rahman

@RahmanLab

small molecules enthusiast; loves ion channels & Fender Stratocaster; a dabbler in drawing; views my own https://t.co/za3Gxnq5xd

Katılım Ekim 2015
795 Takip Edilen924 Takipçiler
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Taufiq Rahman
Taufiq Rahman@RahmanLab·
If you qualify for this scheme and have active research interest in ion channels (any), calcium signalling and/or rational drug design, happy to hear from you: wellcome.org/research-fundi…
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Taufiq Rahman
Taufiq Rahman@RahmanLab·
@sophionbio an awesome meeting (as always)! can't thank Sophion enough for it
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Sophion Bioscience A/S
Sophion Bioscience A/S@sophionbio·
That’s a wrap on ICMS UK 2026. Over two days, ICMS once again brought together the ion channel community to share ideas, reconnect, and spark new collaborations. We would like to thank our speakers and chairs of day. Next ICMS US 2026 is in New York: sophion.com/news-events/io…
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Taufiq Rahman
Taufiq Rahman@RahmanLab·
I am very, very pleased to find this great work from Karakas and colleagues confirming and capturing IP3R2 cluster triggered by IP3: #Sec23" target="_blank" rel="nofollow noopener">nature.com/articles/s4146…. It reminds me of my own work on IP3R3 clustering many years back: nature.com/articles/natur…
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Shozeb Haider
Shozeb Haider@shozeb_haider·
Celebrating Prof Stephen Neidle’s 80th Birthday at the symposium @School_Pharmacy with @DrZoeWaller Gary Parkinson and many other wonderful students, colleagues and collaborators.
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Alzheimer's Society
Alzheimer's Society@alzheimerssoc·
'I’m truly bowled over by the outpouring of support and affection since revealing my dementia diagnosis. 'Receiving a dementia diagnosis can turn your world upside down, but I really do believe it’s better to know. 'Too many people are experiencing delays in diagnosis - on average 3.5 years - meaning they’re left in limbo without the help they need. 'An early diagnosis can open the door to treatment, support, care and the chance to take part in research that could change the future.  'People living with dementia and their families have waited long enough for change. We must demand better for everyone affected. 'I would urge everyone to join me in signing Alzheimer’s Society’s open letter calling on government to deliver a bold and ambitious plan for dementia.’ @jonsnowC4
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Cambridge University
Cambridge University@Cambridge_Uni·
Want to help shape the future of Cambridge? 🧐 Join students from across the University for the Cambridge Student Summit – a day of interactive discussions, workshops, and student-led conversations with local leaders and community organisations. 📅 Thursday 18 June, 9.30am–4pm
 📍 Cambridge Guildhall
 🎫 Free to attend (limited spaces available)
 🍴 Lunch and refreshments provided Book your place now 👉 bit.ly/4dPUnAA
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UN Development
UN Development@UNDP·
Indigenous Peoples are at the 💚 of protecting some of the most vital ecosystems on Earth. They live on and manage roughly 22% of the world’s land, territories that overlap with many of the planet’s most biodiverse and ecologically intact areas. go.undp.org/qs5
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United Nations
United Nations@UN·
We may speak thousands of languages, but we all call this planet home. No matter where we come from, protecting our Earth is a shared responsibility. We need more ambitious #ClimateAction — for our planet and the generations to come. — via @UNDP
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Biology+AI Daily
Biology+AI Daily@BiologyAIDaily·
A unified ensemble-allosteric framework reconciles gain- and loss-of-function disease mutations in the IP3 receptor 1. The study proposes a single ensemble-allosteric model to explain why nearby missense mutations in IP3R1 can cause opposite phenotypes (gain-of-function vs loss-of-function) while the N-terminal fold remains largely intact. 2. By combining in silico saturation mutagenesis with ProteinMPNN/ThermoMPNN and AlphaMissense, pathogenic substitutions are shown to cluster in a “stability-preserving but locally incompatible” regime: mutations tend to disrupt local sequence–structure compatibility without strongly destabilizing the global N-terminal architecture. 3. This reframes IP3R1 channelopathy: disease is driven less by unfolding or structural collapse, and more by corruption of conformational probabilities and allosteric information flow linking ligand recognition to gating. 4. Using BioEmu to sample 1,000 conformations per variant (filtered to retain native-like SD–IBC architecture), the IP3-binding pocket is shown to occupy a discrete multi-basin conformational landscape. Clustering in a pocket-local UMAP embedding identifies three reproducible pocket substates (A–C). 5. Loss-of-function variants tend to reweight these pre-existing pocket substates rather than creating entirely new structures. The LOF mutation R269W shows the strongest redistribution, markedly enriching a rare pocket substate and depleting the WT-dominant one. 6. Pocket physicochemistry explains the R269W LOF mechanism: replacing a cationic IP3-coordinating Arg with bulky Trp reduces pocket volume, lowers positive/charge character, and increases hydrophobicity—changes that are unfavorable for binding a highly phosphorylated ligand like IP3. 7. Adaptive MD (2 μs aggregate per system) plus Markov state models reveal that WT pocket dynamics form a connected three-state kinetic network with efficient exchange. R269W preserves three metastable states but reroutes transitions: exchange from a minor to dominant basin becomes predominantly intermediate-mediated, reducing direct kinetic connectivity between key pocket basins. 8. In contrast, the GOF suppressor-domain mutation R36C keeps a broadly WT-like pocket ensemble and more WT-like pocket kinetics, arguing that GOF does not require local pocket “activation” or collapse. Instead, its effect is distal and allosteric. 9. Contact-informed dynamical network analysis links R36C GOF to weakened suppressor-domain restraint: SD-to-pocket communication is redistributed onto longer, less efficient pathways (increased weighted shortest-path cost), with rewiring of residues/edges near pocket-adjacent loops and altered community organization—consistent with allosteric decoupling rather than pocket failure. 📜Paper: biorxiv.org/content/10.648… #ComputationalBiology #MolecularDynamics #Allostery #ProteinEnsembles #MarkovStateModels #CalciumSignaling #Neurogenetics #IP3R #ITPR1 #VariantInterpretation
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Cambridge University
Cambridge University@Cambridge_Uni·
Wishing a happy Eid al-Adha to all our students, staff, alumni and friends celebrating in Cambridge and around the world 🌙
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The Nobel Prize
The Nobel Prize@NobelPrize·
Today we wish Bob Dylan a happy 85th birthday. Listen to this excerpt from Dylan's Nobel Prize lecture where he reflects on the literary influences that shaped his songwriting. Classic works like 'Moby-Dick', 'All Quiet on the Western Front', and 'The Odyssey' informed his understanding of storytelling and human nature. Hear the full lecture: bit.ly/4kI1Qm5
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Taufiq Rahman
Taufiq Rahman@RahmanLab·
very pleased to see this online near-final version. Really enjoyed collaborating with the Moreno group on this exciting project and glad that I could contribute nature.com/articles/s4146…
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Cambridge University
Cambridge University@Cambridge_Uni·
Thinking about postgraduate study at Cambridge as an international student? 🤔 Our international postgraduate funding webinar series is a deep dive into our scholarships and awards available to international students, including opportunities from Cambridge Trust, Gates Cambridge, and regional partners. Don't miss the opportunity to understand your funding options and join the session in your time zone! ⏰ Register today through the link 👉 bit.ly/4eNxrTz #CambridgeUniversity #Cambridge #Postgraduate
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