Don't listen to this welcomist - don't come to the Baltics! We racist af. We hate you already. Especially, if you're a non-White quasi-human bioid.

Mitochondria Touch the Nuclear Pore: A New Organelle Communication Axis For decades, mitochondria and the nucleus were thought to communicate primarily through signaling molecules, metabolites, and transcriptional feedback loops. A new Nature study reveals something far more direct: 🧬 Mitochondria physically dock onto the nuclear pore complex (NPC). The work identifies a previously unknown organelle contact site where mitochondria interact directly with the nuclear pore through a molecular tether: VDAC1 ↔ RANBP2 (NUP358) This interaction regulates nuclear energy supply, chromatin accessibility, phosphorylation signaling, and ultimately cellular differentiation. A new mitochondria–nucleus contact site Using: 🔬 Super-resolution microscopy 🔬 Electron microscopy 🔬 GST pull-down proteomics 🔬 BioID proximity labeling the authors demonstrated that mitochondria frequently localize adjacent to nuclear pores in multiple tissues including: ❤️ Cardiomyocytes 🧠 Neurons 🫀 Mesenchymal cells 🧫 Cultured fibroblasts. Electron micrographs on pages 2–3 show mitochondria positioned directly against NPC-associated filament structures, rather than merely near the nuclear envelope. This architecture appears evolutionarily conserved across tissues and developmental stages. VDAC1 is the mitochondrial docking protein Two independent proteomic screens converged on the same target: 🎯 VDAC1 the major mitochondrial outer membrane channel. The nuclear binding partner was identified as: 🎯 RANBP2/NUP358 the giant cytoplasmic filament nucleoporin of the nuclear pore complex. Structural modeling identified a direct interaction between: • VDAC1 E50-T51-T52 and • RANBP2 F2977-D2978 creating a molecular bridge between mitochondria and the NPC. Mutating either interface disrupted the interaction. The surprising function: feeding energy directly to the nucleus The most important finding is not structural. It is metabolic. The authors discovered that NPC-associated mitochondria create a privileged energy delivery system to the nucleus. When RANBP2 was deleted: ⬇ Nuclear ATP ⬇ Nuclear phosphocreatine (PCr) ⬇ Nuclear phosphorylation while total cellular ATP remained unchanged. This indicates a: nuclear-specific energetic deficiency rather than global mitochondrial failure. A phosphocreatine shuttle across the nuclear pore One of the most novel aspects of the study is the proposed: ⚡ Mitochondria → phosphocreatine → nucleus shuttle. The model is: Mitochondrial ATP → mitochondrial creatine kinase → phosphocreatine (PCr) → transport through VDAC1–RANBP2 contact region → nuclear creatine kinase → ATP regeneration inside the nucleus. The schematic on Extended Data Fig. 9 (page 34) illustrates this pathway directly. Nuclear signaling collapses without the tether Loss of the VDAC1–RANBP2 interaction caused: ⬇ CREB phosphorylation ⬇ Nuclear phosphoproteome ⬇ Chromatin accessibility ⬇ Developmental transcriptional programs. ATAC-seq revealed widespread chromatin closure. RNA-seq demonstrated suppression of: 🧬 SMAD 🧬 GATA 🧬 FOX 🧬 TBX developmental networks. The strongest affected pathways involved: • differentiation • organ development • cardiac development • neurogenesis. Stem cells fail to differentiate Functional consequences were dramatic. RANBP2-deficient cells showed: ❌ Reduced myotube formation ❌ Reduced adipocyte differentiation ❌ Reduced lineage marker expression. Similarly, human iPSCs carrying: 🧬 VDAC1 interaction mutations or 🧬 RANBP2 C-terminal truncations failed to properly activate cardiomyocyte differentiation programs. Markers including: • ISL1 • NKX2.5 • MEF2C • MYH6 were significantly reduced. Embryos cannot survive without the tether The strongest evidence came in vivo. The investigators generated mice lacking the RANBP2 C-terminal domain responsible for VDAC1 interaction. Result: ☠ Embryonic lethality. Affected embryos developed: ❤️ Thin ventricular myocardium 🧠 Neural tube defects 📉 Reduced neuronal differentiation 📉 Developmental delay. Electron microscopy confirmed increased distance between mitochondria and nuclear pores in mutant embryos. A new paradigm for organelle biology Traditionally: Mitochondria → ATP production → diffusion → nuclear utilization was considered sufficient. This study suggests something much more spatially organized: Energy delivery occurs through dedicated organelle contact sites. The proposed pathway becomes: VDAC1–RANBP2 tether → mitochondrial docking at NPC → local ATP/PCr transfer → nuclear phosphorylation → chromatin remodeling → developmental gene expression → differentiation. Why this matters This work expands the growing field of inter-organelle communication beyond: • mitochondria–ER contacts • mitochondria–lysosome contacts • mitochondria–lipid droplet contacts by establishing: 🎯 mitochondria–nuclear pore contacts as a distinct functional signaling and metabolic hub. The implications extend well beyond development. Potential future relevance includes: 🧠 Aging ❤️ Heart failure 🧬 Stem-cell biology 🦠 Cancer metabolism ⚡ Nuclear bioenergetics 🧬 Epigenetic regulation. The discovery suggests that mitochondrial positioning—not merely mitochondrial activity—can determine nuclear function and cell fate. Reference Menendez-Montes I, Marin-Vicente C, Mukherjee S, et al. Mitochondria directly interact with the nuclear pore complex. Nature (2026) DOI: 10.1038/s41586-026-10588-3 #Mitochondria #NuclearPoreComplex #RANBP2 #VDAC1 #CellDifferentiation #StemCells #CardiacDevelopment #Neurodevelopment #ChromatinBiology #NatureJournal

Ik geef aan dat stablecoins programmeerbaar en de voorloper al dan niet de CBDCs zelf zijn die door private bedrijven worden uitgegeven onder goedkeuring van nu nog overheden. Gekoppeld aan een BIOID en bijvoorbeeld een CO2ID. Maakt niet uit in welke wallet ze zitten.

Why would China, North Korea, Iran, Palestine, and Russia implement something that Zionists or Israel want? Are you claiming that these countries are weak and can be led and controlled by Zionist and Israel? Type "Trump slows down the global turnkey" into Google and ask yourself why the UN (BIMS) and the UN program (SCOPE) refuse food and aid to refugees in various countries if they refuse a BioID. Look into the palm vein program. We literally fund it with the global world’s taxes. Also ask yourself why Trump officially blocked the creation of a government-run digital currency by signing Executive Order 14178 on January 23, 2025.

HelixKey: Biometric Identity for Web3 Seed phrases get lost. HelixKey replaces them with biometric proofs. Your face → Zero-Knowledge Proof → On-Chain BioID. No secret. No theft. No coercion. What's live: Testnet contracts, multi-chain bridges, DNA keys coming Phase 2. We're diving deep into this infrastructure—and we'll be partnering with them very soon. More details coming. Stay tuned. @HelixKeyBio

Researchers present BioID proximity proteomes of the #Parkinsons-associated protein LRRK2 that reveal new interactors, which they further characterize using a novel evolutionary & structural bioinformatics pipeline link.springer.com/article/10…

Tyvärr har jag blivit så skadad att jag tror att enda anledningen media skriver om detta är att vi ska bli så himla tacksamma att Ai/BioID kommer att fixa problemet. Det gamla vanliga Problem-Reaction-Solution grejen.

🇸🇪 Linköping University | PhD in Data-Driven Cell & Molecular Biology 🧬💻 A PhD position is open at Linköping University, focusing on AI-driven modeling of protein interactions in cancer biology. 📌 Position Overview 🎓 Role: PhD Student in Data-driven Cell and Molecular Biology 📍 Location: Linköping 🏢 Department: Bioinformatics and Computational Biology (IFM) 👩‍🏫 Supervisor: Maria Sunnerhagen 💼 Type: Full-time ⏳ Duration: 4 years (extendable up to 5 years) 📅 Start: As agreed ⏳ Deadline: May 28, 2026 🔬 Research Focus This PhD explores data-driven and AI-based modeling of intrinsically disordered proteins (IDPs) and their role in cancer-related protein interaction networks. The project combines mass spectrometry data (BioID), computational modeling, and experimental validation to understand how dynamic protein interactions regulate key biological processes. The goal is to develop predictive pipelines for molecular interaction modeling, enabling new strategies to target protein interactions in cancer. 🛠️ Key Responsibilities Develop computational pipelines, analyze protein interaction data, apply AI/ML techniques, collaborate with experimental labs, and contribute to interdisciplinary research across institutions. 🎯 Ideal Candidate Master’s degree in bioinformatics, computational biology, physics, or related field. Strong programming skills (Python), interest in AI/ML, and background in structural biology or molecular modeling are highly desirable. 🌟 Why Apply? Be part of the prestigious Data-Driven Life Science (DDLS) program, collaborate internationally (including with University of Toronto), and work at the intersection of AI, biology, and cancer research. 🌍 Location Linköping offers a modern, student-friendly environment with strong research infrastructure and a high quality of life in Sweden. 🔗 More Info phdscanner.com/opportunities… #PhD #Sweden #Bioinformatics #ComputationalBiology #AI #MachineLearning #CancerResearch #LifeSciences #Research

Mini memory modules of BioID data related to exact booth strength. Standalone mini Aadhar database. This may be a technical challenge rather than feasibility problem.

Yes sir, but it's a major rework. I support Bio Verification in principle but considering our geographical realities we need 100% 4G-5G coverage. Also ensure new set of IP protocols to sustain interference free network. Another simple solution, localised BioID data in mini chips

RRAS2 #AbdominalAorticAneurysm RRAS2 in 👤aortic Smooth Muscle Cell ⏫pY248 TFII-I ⏫contractile genes ⏬proliferation migration apoptosis BioID for RRAS2 interactome▶️MET TTK BRAF WNK1 PASK TESK2 TAOK3 Ang II▶️⏬ MEG3 ▶️⏬RRAS2 CLIP-seq RNA-binding protein of MEG3 MEG3 pull down-MS CatRAPID predicted RRAS2 binding proteins▶️ ELAVL1▶️ ⏫RRAS2 mRNA stability SM22 SMC Rras2 KO🐭 Ang II or elastase ⏫AAA loss of contractile SMCs rescued by Lenti-LoxP-Rras2 AAV9-SM22-MEG3 ⏬AAA (Ang II) @NatureComms 2025 nature.com/articles/s41467-0…

1. Excel to identify all defects 2. Python with opencv or, BIOID or Xeoma to match face and create identifier and isolate defect. 3. Individual and selective biometric corrections for defects. You see how your brain couldn’t fanthom this and easily swayed by political rhetoric

Funny, I was thinking I should check into data breeches with pcOptimum because they don't allow point redemption online currently and I was randomly logged out. Just, didn't yet, so thank you! The digital security crisis is getting closer, I suspect. Get your BioID ready. 🫤

You can’t be talking like that bioid

これまで原因不明の神経疾患とされていた病気が、「ニューロンのリソソームからの糖の運び出し不良」による「新しいタイプのリソソーム病」として定義。 脳は、人体の中で最も精緻かつ複雑な臓器であり、その機能は多様な細胞種の協調的な相互作用によって維持されている。 神経細胞（ニューロン）による電気化学的な情報伝達、アストロサイトによる代謝的・構造的サポート、オリゴデンドロサイトによる髄鞘形成、そしてミクログリアによる免疫監視と貪食作用など、それぞれの細胞種は極めて特化した機能を担っている 。 中でも「リソソーム」は、細胞内の分解・リサイクル工場として、またmTORC1シグナル伝達のハブとして、細胞の恒常性維持に不可欠な役割を果たしている 。 リソソームの機能不全は、アルツハイマー病やパーキンソン病といった主要な神経変性疾患、およびリソソーム病（Lysosomal Storage Disorders: LSDs）と呼ばれる遺伝性代謝疾患の共通した病理学的基盤である 。 しかし、これまで「ニューロンのリソソーム」と「ミクログリアのリソソーム」が、その構成タンパク質や機能においてどのように異なるのか、またその違いがどのように疾患感受性に関与しているのかを体系的に解明した研究は存在しなかった。 リソソーム膜タンパク質TMEM192に3xHAタグを融合させたLysoTagを、細胞種特異的プロモーター（Syn1: ニューロン, Gfap: アストロサイト, Olig2: オリゴデンドロサイト, Cx3cr1/Fcrls: ミクログリア）下で発現させるトランスジェニックマウスを作出 磁気ビーズを用いた迅速な免疫沈降によりインタクトなリソソームを単離し、データ非依存的取得（DIA）質量分析法を用いて高深度かつ定量的なプロテオーム解析を実施 結果１：解析の結果、790種類のリソソーム濃縮タンパク質が同定され、そのうち487種類は従来リソソーム局在がアノテーションされていない新規候補 結果２：知的障害・てんかんの原因遺伝子SLC45A1が、ニューロンのリソソームに特異的に局在する。SLC45A1欠損細胞およびKOマウスのリソソーム内にヘキソース（グルコース等）の顕著な蓄積が確認された。これはSLC45A1がリソソームからの糖排出トランスポーターであることを証明している。 結果３：BioIDおよびCo-IP解析により、SLC45A1がV-ATPaseのV1セクターと相互作用することが判明した。SLC45A1の欠損は、飢餓ストレス下でのV1セクターのリソソーム膜への集合を阻害し、リソソームpHの上昇（酸性化不全）を引き起こした。 SLC45A1関連疾患を、糖輸送障害とV-ATPase安定性低下を主因とする「新規のニューロン特異的リソソーム病」として再定義 細胞種特異的リソソームアトラスの構築は新しい情報として有用そう。だけど、その結果を変に理解して、民間リソソーム治療とかが出てきそう。 cell.com/cell/fulltext/S0092…

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Bioid

Twitter (X) -free Geetanjali is at the annual meeting of the Indian Society for Cell Biology at IIT Kanpur, presenting her poster on using BioID to find novel receptors for the transit peptide of apicoplast proteins. @IITKanpur

Sabrina Wallace BioID 3 ~ (featuring Dr. Group) February 20, 2025 odysee.com/@CorinneNokel:b/B…

Sabrina Wallace BioID 3 ~ (featuring Dr. Group) February 20, 2025 odysee.com/@CorinneNokel:b/B…