🔬 Exciting News from Our Recent Paper! 🔬
📚 Title: In silico study of the impact of oxidation on pyruvate transmission across the hVDAC1 protein channel
Our recently published paper delves into the fascinating realm of cancer cell metabolism, focusing on the pivotal role of Voltage Dependent Anion Channels (VDACs), particularly VDAC1. Here's a snapshot of our findings:
🔍 Objective: Investigating the Effect of Low-Level VDAC1 Oxidation on Pyruvate Uptake
🧪 Methodology: Leveraging Molecular Dynamics (MD) Simulations
👉 Key Insights:
The overexpression of VDACs, especially VDAC1, in cancer cells compared to normal cells, has long been recognized. In our study, we honed in on the impact of a low level of VDAC1 oxidation, induced by Cold Atmospheric Plasma (CAP), on pyruvate (Pyr) uptake. Inhibiting Pyr uptake through VDAC1 emerges as a potential strategy to suppress cancer cell proliferation.
💡 Significant Findings:
Employed MD simulations to analyze hVDAC1 structure with modified cysteine and methionine residues.
Results indicated that the free energy barrier for Pyr translocation through the oxidized channel was significantly higher compared to the native channel.
Specifically, the barrier for Pyr translocation through the native channel was approximately 4.3 ± 0.7 kJ mol−1, while for the oxidized channel, it rose to 10.8 ± 1.8 kJ mol−1.
Higher barrier in the oxidized channel correlates with a decreased rate of Pyr permeation, suggesting a potential mechanism for inhibiting cancer cell proliferation.
🌐 Broader Implications:
Our findings unveil that low levels of CAP-induced oxidation reduce Pyr translocation, thereby curbing cancer cell proliferation. This suggests that subtle oxidative modifications may hold therapeutic potential in treating cancer cells by disrupting crucial metabolic pathways.
🚀 Future Directions:
Our research lays the groundwork for further exploration of CAP-induced oxidation as a targeted approach in cancer treatment. As we unravel the intricate connections between VDAC1, Pyr uptake, and cancer cell metabolism, we pave the way for innovative strategies in the fight against cancer.
🙌 Acknowledgments:
Kudos to our dedicated team for their commitment to advancing scientific knowledge and contributing to the ongoing discourse in cancer research. Together, we are shaping the future of cancer treatment!
#CancerResearch #ScienceBreakthrough #MolecularDynamics #ColdPlasma #InnovationInHealthcare #ResearchPublication
📚 Title: In silico study of the impact of oxidation on pyruvate transmission across the hVDAC1 protein channel
Our recently published paper delves into the fascinating realm of cancer cell metabolism, focusing on the pivotal role of Voltage Dependent Anion Channels (VDACs), particularly VDAC1. Here's a snapshot of our findings:
🔍 Objective: Investigating the Effect of Low-Level VDAC1 Oxidation on Pyruvate Uptake
🧪 Methodology: Leveraging Molecular Dynamics (MD) Simulations
👉 Key Insights:
The overexpression of VDACs, especially VDAC1, in cancer cells compared to normal cells, has long been recognized. In our study, we honed in on the impact of a low level of VDAC1 oxidation, induced by Cold Atmospheric Plasma (CAP), on pyruvate (Pyr) uptake. Inhibiting Pyr uptake through VDAC1 emerges as a potential strategy to suppress cancer cell proliferation.
💡 Significant Findings:
Employed MD simulations to analyze hVDAC1 structure with modified cysteine and methionine residues.
Results indicated that the free energy barrier for Pyr translocation through the oxidized channel was significantly higher compared to the native channel.
Specifically, the barrier for Pyr translocation through the native channel was approximately 4.3 ± 0.7 kJ mol−1, while for the oxidized channel, it rose to 10.8 ± 1.8 kJ mol−1.
Higher barrier in the oxidized channel correlates with a decreased rate of Pyr permeation, suggesting a potential mechanism for inhibiting cancer cell proliferation.
🌐 Broader Implications:
Our findings unveil that low levels of CAP-induced oxidation reduce Pyr translocation, thereby curbing cancer cell proliferation. This suggests that subtle oxidative modifications may hold therapeutic potential in treating cancer cells by disrupting crucial metabolic pathways.
🚀 Future Directions:
Our research lays the groundwork for further exploration of CAP-induced oxidation as a targeted approach in cancer treatment. As we unravel the intricate connections between VDAC1, Pyr uptake, and cancer cell metabolism, we pave the way for innovative strategies in the fight against cancer.
🙌 Acknowledgments:
Kudos to our dedicated team for their commitment to advancing scientific knowledge and contributing to the ongoing discourse in cancer research. Together, we are shaping the future of cancer treatment!
#CancerResearch #ScienceBreakthrough #MolecularDynamics #ColdPlasma #InnovationInHealthcare #ResearchPublication
The beginning of 2024 brings positive news as our research achieves publication in the ACS Journal of Chemical Theory and Computation. 📚🎉 https://pubs.acs.org/doi/10.1021/acs.jctc.3c01020
🔬 Exploring the Secrets of BH4–: Bridging the Gap Between Experiment and Simulation 🌐
The borohydride ion, BH4–, plays a crucial role as a reducing agent in various technological processes. However, unraveling its mysteries has been challenging due to stability issues in aqueous solutions and its unique hydration shell.
🧪 In our latest study, we've taken a multidisciplinary approach, combining experiments and computer simulations. Overcoming the limitations posed by BH4–'s instability, we measured its activity coefficient and delved into its solvation free energies using quantum chemical calculations.
💻 This innovative strategy has allowed us to develop a classical force field for NaBH4, enriching our understanding of its characteristics. The force field accurately captures solvation free energy, hydration structure, and the activity coefficient, providing valuable insights for molecular dynamics simulations.
🌊 These findings pave the way for more accurate modeling of BH4– interactions, influencing its role in diverse scenarios.
#ScientificDiscovery #ChemistryResearch #BH4Ion #MolecularDynamics #SimulationInsights
🔬 Exploring the Secrets of BH4–: Bridging the Gap Between Experiment and Simulation 🌐
The borohydride ion, BH4–, plays a crucial role as a reducing agent in various technological processes. However, unraveling its mysteries has been challenging due to stability issues in aqueous solutions and its unique hydration shell.
🧪 In our latest study, we've taken a multidisciplinary approach, combining experiments and computer simulations. Overcoming the limitations posed by BH4–'s instability, we measured its activity coefficient and delved into its solvation free energies using quantum chemical calculations.
💻 This innovative strategy has allowed us to develop a classical force field for NaBH4, enriching our understanding of its characteristics. The force field accurately captures solvation free energy, hydration structure, and the activity coefficient, providing valuable insights for molecular dynamics simulations.
🌊 These findings pave the way for more accurate modeling of BH4– interactions, influencing its role in diverse scenarios.
#ScientificDiscovery #ChemistryResearch #BH4Ion #MolecularDynamics #SimulationInsights
ACS Publications
Unveiling the Borohydride Ion through Force-Field Development
The borohydride ion, BH4–, is an essential reducing agent in many technological processes, yet its full understanding has been elusive, because of at least two significant challenges. One challenge arises from its marginal stability in aqueous solutions outside…
α-sinuklein fibril shakllanishini erta bosqichlarda to'xtatish PDni kuchayib borayotgan va patogen α-sinuklein fibrillarining hosil bo'lishini to'xtatish orqali kurashishning samarali yechimi bo'lishi mumkin. 🌟🧬🛡 https://www.sciencedirect.com/science/article/abs/pii/S1047847724000492
#ParkinsonsDisease #NeurodegenerativeDisorders #MolecularDynamics #Research #AlphaSynuclein #ElectricField #EarlyIntervention #ScientificDiscovery #HealthInnovation #BiomedicalResearch
#ParkinsonsDisease #NeurodegenerativeDisorders #MolecularDynamics #Research #AlphaSynuclein #ElectricField #EarlyIntervention #ScientificDiscovery #HealthInnovation #BiomedicalResearch
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[UZ] 🌟 Ilmiy tadqiqotlarimizdan ajoyib yangilik! 🌟
Alzheimer kasalligi (AD) bo‘yicha yangi tadqiqotimiz, dunyo bo‘ylab millionlab insonlarga ta'sir qiluvchi og‘ir nevrodejenerativ kasallik, Nature nashryotining Scientific Reports jurnalida chop etildi. 🧠✨
Ushbu tadqiqotda biz statik va o’zgaruvchan elektr maydonlari Alzheimer kasalligi bilan bog‘liq bo‘lgan zararli Aβ fibrillarini qanday buzishini o‘rgandik. Molekulyar dinamika simulyatsiyalari yordamida, toksikligi va barqaror tuzilishi bilan mashhur bo‘lgan Osaka mutatsiyasi (E22Δ) ga ega Aβ1–40 peptidining polimorfik fibril kompleksini tadqiq qildik.
Tadqiqot natijalarimiz shuni ko‘rsatadiki, 0.3–0.4 V/nm elektr maydoni va 0.20 GHz chastota bilan bu zararli fibrillarni samarali ravishda buzish mumkin. Bu yondashuv Alzheimer kasalligini davolash bo‘yicha yangi terapevtik usullarni ochib berishi mumkin. 🔬⚡️
Ushbu tadqiqotda ko‘rsatgan qimmatli hissalari uchun Dr. Artyom Baev (Ilg’or texnologiyalar markazi), Dr. Erkin S Kurganov (Broad Institute of MIT and Harvard), va fidoyi magistr talabam Muhriddin Mahkamovga katta rahmat aytaman.
To‘liq maqolani bu yerda o‘qing: https://www.nature.com/articles/s41598-024-72778-1
(Mana nima uchun mahalliy va xalqaro hamkorlik kerak!!!)
[EN] 🌟 Exciting Research Update! 🌟
Our latest study on Alzheimer’s disease (AD), a devastating neurodegenerative disorder affecting millions worldwide, has been published in Nature’s Scientific Reports. 🧠✨
In this research, we explored how static and oscillating electric fields can disrupt the harmful Aβ fibrils associated with AD. Using molecular dynamics simulations, we specifically examined a polymorphic fibrillar complex of the Aβ1–40 peptide with the Osaka mutation (E22Δ), which is known for its toxicity and stable structure.
Our findings reveal that applying a 0.3–0.4 V/nm electric field at a 0.20 GHz frequency can effectively disrupt these toxic fibrils, potentially offering a novel therapeutic approach to combating AD pathology. This is a promising step forward in understanding and addressing Alzheimer’s disease. 🔬⚡️
A huge thank you to Dr. Artyom Baev, Dr. Erkin Kurganov, and my dedicated student Mukhriddin Makhkamov for their valuable contributions to this work.
#AlzheimersResearch #NeurodegenerativeDisorders #MolecularDynamics #Therapeutics #ScientificReports #ElectricFields #ResearchInnovation #ADPathology
Alzheimer kasalligi (AD) bo‘yicha yangi tadqiqotimiz, dunyo bo‘ylab millionlab insonlarga ta'sir qiluvchi og‘ir nevrodejenerativ kasallik, Nature nashryotining Scientific Reports jurnalida chop etildi. 🧠✨
Ushbu tadqiqotda biz statik va o’zgaruvchan elektr maydonlari Alzheimer kasalligi bilan bog‘liq bo‘lgan zararli Aβ fibrillarini qanday buzishini o‘rgandik. Molekulyar dinamika simulyatsiyalari yordamida, toksikligi va barqaror tuzilishi bilan mashhur bo‘lgan Osaka mutatsiyasi (E22Δ) ga ega Aβ1–40 peptidining polimorfik fibril kompleksini tadqiq qildik.
Tadqiqot natijalarimiz shuni ko‘rsatadiki, 0.3–0.4 V/nm elektr maydoni va 0.20 GHz chastota bilan bu zararli fibrillarni samarali ravishda buzish mumkin. Bu yondashuv Alzheimer kasalligini davolash bo‘yicha yangi terapevtik usullarni ochib berishi mumkin. 🔬⚡️
Ushbu tadqiqotda ko‘rsatgan qimmatli hissalari uchun Dr. Artyom Baev (Ilg’or texnologiyalar markazi), Dr. Erkin S Kurganov (Broad Institute of MIT and Harvard), va fidoyi magistr talabam Muhriddin Mahkamovga katta rahmat aytaman.
To‘liq maqolani bu yerda o‘qing: https://www.nature.com/articles/s41598-024-72778-1
(Mana nima uchun mahalliy va xalqaro hamkorlik kerak!!!)
[EN] 🌟 Exciting Research Update! 🌟
Our latest study on Alzheimer’s disease (AD), a devastating neurodegenerative disorder affecting millions worldwide, has been published in Nature’s Scientific Reports. 🧠✨
In this research, we explored how static and oscillating electric fields can disrupt the harmful Aβ fibrils associated with AD. Using molecular dynamics simulations, we specifically examined a polymorphic fibrillar complex of the Aβ1–40 peptide with the Osaka mutation (E22Δ), which is known for its toxicity and stable structure.
Our findings reveal that applying a 0.3–0.4 V/nm electric field at a 0.20 GHz frequency can effectively disrupt these toxic fibrils, potentially offering a novel therapeutic approach to combating AD pathology. This is a promising step forward in understanding and addressing Alzheimer’s disease. 🔬⚡️
A huge thank you to Dr. Artyom Baev, Dr. Erkin Kurganov, and my dedicated student Mukhriddin Makhkamov for their valuable contributions to this work.
#AlzheimersResearch #NeurodegenerativeDisorders #MolecularDynamics #Therapeutics #ScientificReports #ElectricFields #ResearchInnovation #ADPathology
Nature
Understanding Osaka mutation polymorphic Aβ fibril response to static and oscillating electric fields: insights from computational…
Scientific Reports - Understanding Osaka mutation polymorphic Aβ fibril response to static and oscillating electric fields: insights from computational modeling
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🧬📢 Navbatdagi hamkorlikdagi ilmiy maqolamiz ACS Journal of Chemical Information and Modeling jurnalida chop etildi! (IF- 5.7)🎉
Ushbu tadqiqot Center for Advanced Technologies - CAT Ilg'or texnologiyalar markazi - ITM olimlari bilan olib borayotgan mustahkam hamkorligimiz samarasidir. Ayniqsa, Artyom Baev rahbarligidagi guruhdagi iqtidorli yosh tadqiqotchi Khondamir Rustamovning o‘rni beqiyos — u sun’iy intellekt asosidagi molekulyar modellashtirish bo‘yicha ajoyib natijalarga erishib kelmoqda! 🚀🧠
🔍 Inson organizmidagi eng muhim o‘smaga qarshi oqsillardan biri — p53 o'rganildi. Bu oqsil saratonlarning 50% dan ortig‘ida mutatsiyaga uchraydi.
AlphaFold3, molekulyar dinamikaga asoslangan simulyatsiyalar orqali p53 ning 148 ta missens mutatsiyasini chuqur tahlil qilingan.
🔑 Tadqiqotdan asosiy natijalar:
- Ba’zi mutatsiyalar (masalan, R248P, N239S) DNK bilan bog‘lanish qobiliyatini kamaytiradi,
- Boshqalari (C238Y, P278R) esa bog‘lanishni kuchaytiradi, lekin sistemani beqarorlashtiradi,
- Qiziqarli tomoni shundaki, E285A, M243T kabi mutatsiyalar zararli ta’sirni kamaytirish (rescue) xususiyatiga ega bo‘lishi mumkin.
Tadqiqotimiz AI va hisoblash usullari yordamida saraton bilan bog‘liq molekulyar mexanizmlarni chuqur tushunishga imkon beradi 💡💊
🙏 Ushbu muhim tadqiqotda ishtirok etishga taklif qilgan hamkorlarim Artyom va Khondamirga chuqur minnatdorchilik bildiraman.
🧪🌍
🔗 https://pubs.acs.org/doi/abs/10.1021/acs.jcim.5c00580
#ACS #p53 #Cancer #AI #AlphaFold #moleculardynamics #ProteinChallenge #DNA
Ushbu tadqiqot Center for Advanced Technologies - CAT Ilg'or texnologiyalar markazi - ITM olimlari bilan olib borayotgan mustahkam hamkorligimiz samarasidir. Ayniqsa, Artyom Baev rahbarligidagi guruhdagi iqtidorli yosh tadqiqotchi Khondamir Rustamovning o‘rni beqiyos — u sun’iy intellekt asosidagi molekulyar modellashtirish bo‘yicha ajoyib natijalarga erishib kelmoqda! 🚀🧠
🔍 Inson organizmidagi eng muhim o‘smaga qarshi oqsillardan biri — p53 o'rganildi. Bu oqsil saratonlarning 50% dan ortig‘ida mutatsiyaga uchraydi.
AlphaFold3, molekulyar dinamikaga asoslangan simulyatsiyalar orqali p53 ning 148 ta missens mutatsiyasini chuqur tahlil qilingan.
🔑 Tadqiqotdan asosiy natijalar:
- Ba’zi mutatsiyalar (masalan, R248P, N239S) DNK bilan bog‘lanish qobiliyatini kamaytiradi,
- Boshqalari (C238Y, P278R) esa bog‘lanishni kuchaytiradi, lekin sistemani beqarorlashtiradi,
- Qiziqarli tomoni shundaki, E285A, M243T kabi mutatsiyalar zararli ta’sirni kamaytirish (rescue) xususiyatiga ega bo‘lishi mumkin.
Tadqiqotimiz AI va hisoblash usullari yordamida saraton bilan bog‘liq molekulyar mexanizmlarni chuqur tushunishga imkon beradi 💡💊
🙏 Ushbu muhim tadqiqotda ishtirok etishga taklif qilgan hamkorlarim Artyom va Khondamirga chuqur minnatdorchilik bildiraman.
🧪🌍
🔗 https://pubs.acs.org/doi/abs/10.1021/acs.jcim.5c00580
#ACS #p53 #Cancer #AI #AlphaFold #moleculardynamics #ProteinChallenge #DNA
ACS Publications
Investigation of Structural Mechanisms Underlying p53 Dysfunction Caused by 148 Missense Mutations Using AlphaFold3 and Molecular…
Tumor protein p53 (TP53) is a crucial regulator of genomic integrity, frequently mutated in more than half of all human cancers. These mutations predominantly target the DNA-binding domain (DBD), impairing p53’s interaction with DNA and its tumor-suppressive…
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