Introduction – Company Background

GuangXin Industrial Co., Ltd. is a specialized manufacturer dedicated to the development and production of high-quality insoles.

With a strong foundation in material science and footwear ergonomics, we serve as a trusted partner for global brands seeking reliable insole solutions that combine comfort, functionality, and design.

With years of experience in insole production and OEM/ODM services, GuangXin has successfully supported a wide range of clients across various industries—including sportswear, health & wellness, orthopedic care, and daily footwear.

From initial prototyping to mass production, we provide comprehensive support tailored to each client’s market and application needs.

At GuangXin, we are committed to quality, innovation, and sustainable development. Every insole we produce reflects our dedication to precision craftsmanship, forward-thinking design, and ESG-driven practices.

By integrating eco-friendly materials, clean production processes, and responsible sourcing, we help our partners meet both market demand and environmental goals.

Core Strengths in Insole Manufacturing

At GuangXin Industrial, our core strength lies in our deep expertise and versatility in insole and pillow manufacturing. We specialize in working with a wide range of materials, including PU (polyurethane), natural latex, and advanced graphene composites, to develop insoles and pillows that meet diverse performance, comfort, and health-support needs.

Whether it's cushioning, support, breathability, or antibacterial function, we tailor material selection to the exact requirements of each project-whether for foot wellness or ergonomic sleep products.

We provide end-to-end manufacturing capabilities under one roof—covering every stage from material sourcing and foaming, to precision molding, lamination, cutting, sewing, and strict quality control. This full-process control not only ensures product consistency and durability, but also allows for faster lead times and better customization flexibility.

With our flexible production capacity, we accommodate both small batch custom orders and high-volume mass production with equal efficiency. Whether you're a startup launching your first insole or pillow line, or a global brand scaling up to meet market demand, GuangXin is equipped to deliver reliable OEM/ODM solutions that grow with your business.

Customization & OEM/ODM Flexibility

GuangXin offers exceptional flexibility in customization and OEM/ODM services, empowering our partners to create insole products that truly align with their brand identity and target market. We develop insoles tailored to specific foot shapes, end-user needs, and regional market preferences, ensuring optimal fit and functionality.

Our team supports comprehensive branding solutions, including logo printing, custom packaging, and product integration support for marketing campaigns. Whether you're launching a new product line or upgrading an existing one, we help your vision come to life with attention to detail and consistent brand presentation.

With fast prototyping services and efficient lead times, GuangXin helps reduce your time-to-market and respond quickly to evolving trends or seasonal demands. From concept to final production, we offer agile support that keeps you ahead of the competition.

Quality Assurance & Certifications

Quality is at the heart of everything we do. GuangXin implements a rigorous quality control system at every stage of production—ensuring that each insole meets the highest standards of consistency, comfort, and durability.

We provide a variety of in-house and third-party testing options, including antibacterial performance, odor control, durability testing, and eco-safety verification, to meet the specific needs of our clients and markets.

Our products are fully compliant with international safety and environmental standards, such as REACH, RoHS, and other applicable export regulations. This ensures seamless entry into global markets while supporting your ESG and product safety commitments.

ESG-Oriented Sustainable Production

At GuangXin Industrial, we are committed to integrating ESG (Environmental, Social, and Governance) values into every step of our manufacturing process. We actively pursue eco-conscious practices by utilizing eco-friendly materials and adopting low-carbon production methods to reduce environmental impact.

To support circular economy goals, we offer recycled and upcycled material options, including innovative applications such as recycled glass and repurposed LCD panel glass. These materials are processed using advanced techniques to retain performance while reducing waste—contributing to a more sustainable supply chain.

We also work closely with our partners to support their ESG compliance and sustainability reporting needs, providing documentation, traceability, and material data upon request. Whether you're aiming to meet corporate sustainability targets or align with global green regulations, GuangXin is your trusted manufacturing ally in building a better, greener future.

Let’s Build Your Next Insole Success Together

Looking for a reliable insole manufacturing partner that understands customization, quality, and flexibility? GuangXin Industrial Co., Ltd. specializes in high-performance insole production, offering tailored solutions for brands across the globe. Whether you're launching a new insole collection or expanding your existing product line, we provide OEM/ODM services built around your unique design and performance goals.

From small-batch custom orders to full-scale mass production, our flexible insole manufacturing capabilities adapt to your business needs. With expertise in PU, latex, and graphene insole materials, we turn ideas into functional, comfortable, and market-ready insoles that deliver value.

Contact us today to discuss your next insole project. Let GuangXin help you create custom insoles that stand out, perform better, and reflect your brand’s commitment to comfort, quality, and sustainability.

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High-performance graphene insole OEM Thailand

Are you looking for a trusted and experienced manufacturing partner that can bring your comfort-focused product ideas to life? GuangXin Industrial Co., Ltd. is your ideal OEM/ODM supplier, specializing in insole production, pillow manufacturing, and advanced graphene product design.

With decades of experience in insole OEM/ODM, we provide full-service manufacturing—from PU and latex to cutting-edge graphene-infused insoles—customized to meet your performance, support, and breathability requirements. Our production process is vertically integrated, covering everything from material sourcing and foaming to molding, cutting, and strict quality control.ODM pillow factory for sleep product brands

Beyond insoles, GuangXin also offers pillow OEM/ODM services with a focus on ergonomic comfort and functional innovation. Whether you need memory foam, latex, or smart material integration for neck and sleep support, we deliver tailor-made solutions that reflect your brand’s values.

We are especially proud to lead the way in ESG-driven insole development. Through the use of recycled materials—such as repurposed LCD glass—and low-carbon production processes, we help our partners meet sustainability goals without compromising product quality. Our ESG insole solutions are designed not only for comfort but also for compliance with global environmental standards.Insole ODM factory in Indonesia

At GuangXin, we don’t just manufacture products—we create long-term value for your brand. Whether you're developing your first product line or scaling up globally, our flexible production capabilities and collaborative approach will help you go further, faster.Taiwan OEM insole and pillow manufacturing factory

📩 Contact us today to learn how our insole OEM, pillow ODM, and graphene product design services can elevate your product offering—while aligning with the sustainability expectations of modern consumers.Innovative insole ODM solutions in Thailand

ARTEMIS, a new machine learning tool by Johns Hopkins researchers, identifies repeat DNA sequences in cancer, enabling noninvasive diagnosis and insights into cancer genetics. It marks a significant advancement in cancer detection and monitoring, with potential applications in early detection and treatment response evaluation. Credit: Carolyn Hruban Identifying and characterizing repeated DNA sequences, sometimes called “junk DNA” or “dark matter” within chromosomes, which may play a role in cancer or other diseases, has proven to be difficult. Now, investigators at the Johns Hopkins Kimmel Cancer Center have developed a novel approach that uses machine learning to identify these elements in cancerous tissue, as well as in cell-free DNA (cfDNA) — fragments that are shed from tumors and float in the bloodstream. This new method could provide a noninvasive means of detecting cancers or monitoring response to therapy. Machine learning is a type of artificial intelligence that uses data and computer algorithms to perform complex tasks and accelerate research. In laboratory tests, the method, called ARTEMIS (Analysis of RepeaT EleMents in dISease) examined over 1,200 types of repeat elements comprising nearly half of the human genome, and identified that a large number of repeats not previously known to be associated with cancer were altered in tumor formation. The investigators also were able to identify changes in these elements in cfDNA, providing a way to detect cancer and determine where in the body it originated. A description of the work is to be published March 13 in Science Translational Medicine. ARTEMIS Unveils the Role of “Dark Genome” in Cancer “When you think about existing cancer genes and the DNA sequences around them, they’re just chock full of these repeats,” says Victor E. Velculescu, M.D., Ph.D., a professor of oncology and co-director of the Cancer Genetics and Epigenetics Program at the Johns Hopkins Kimmel Cancer Center, who led the study with Akshaya Annapragada, an M.D./Ph.D. student at the Johns Hopkins University School of Medicine, and Robert Scharpf, Ph.D., an associate professor of oncology at Johns Hopkins. “Until ARTEMIS, this dark matter of the genome was essentially ignored, but now we’re seeing that these repeats are not occurring randomly,” Velculescu says. “They end up being clustered around genes that are altered in cancer in a variety of different ways, providing the first glimpse that these sequences may be key to tumor development.” In a series of laboratory tests, the researchers first examined the distribution of 1.2 billion kmers (short sequences of DNA) defining unique repeats, finding them enriched in genes commonly altered in human cancers. For example, of 736 genes known to drive cancers, 487 contained an average fifteenfold higher than expected number of repeat sequences. These repeat sequences also were significantly increased in genes involved in cell signaling pathways that are commonly dysregulated in cancers. Using next-generation sequencing, technology that allows researchers to rapidly examine the sequences of entire genomes, the researchers also looked to see if repeat sequences were directly altered in cancers. They used ARTEMIS to analyze over 1,200 distinct types of repeat elements in tumor and normal tissues from 525 patients with different cancers participating in the Pan-Cancer Analysis of Whole Genomes (PCAWG), and found a median of 807 altered elements in each tumor. Nearly two-thirds of these elements (820 of 1,280) had not previously been observed as being altered in human cancers. Then, they used a machine-learning model to generate an ARTEMIS score for each sample to provide a summary of genome-wide repeat element changes that were predictive of cancer. ARTEMIS scores distinguished the 525 PCAWG participants’ tumors from normal tissues with a high performance (AUC=0.96) across all cancer types analyzed, where 1 is a perfect score. Increased ARTEMIS scores were associated with shorter overall and progression-free survival regardless of tumor type. Enhancements in Cancer Detection and Monitoring The investigators next evaluated ARTEMIS’ potential for noninvasive detection of cancer. They applied the tool to blood samples from 287 individuals with and without lung cancer participating in the Danish Lung Cancer Screening Study (LUCAS). ARTEMIS classified patients with lung cancer with an area under the curve (AUC) of 0.82. But when used with another method called DELFI (DNA evaluation of fragments for early interception) — an assay previously developed by Velculescu, Scharpf, and other members of their group that detects changes in the size and distribution of cfDNA fragments across the genome — the combination model classified patients with lung cancer with an AUC of 0.91. Similar performance was observed in a group of 208 individuals at risk for liver cancer, in which ARTEMIS detected individuals with liver cancer among others with cirrhosis or viral hepatitis with an AUC of 0.87. When combined with DELFI, the AUC increased to 0.90. Finally, they evaluated whether the ARTEMIS blood test could identify where in the body a tumor originated in patients with cancer. When trained with information from the PCAWG participants, the tool could classify the source of tumor tissues with an average of 78% accuracy among 12 tumor types. The investigators then combined ARTEMIS and DELFI to assess blood samples from a group of 226 individuals with breast, ovarian, lung, colorectal, bile duct, gastric, or pancreatic tumors. Here, the model correctly classified patients among the different cancer types with an average accuracy of 68%, which improved to 83% when the model was allowed to suggest two possible tumor types instead of a single cancer type. “Our study shows that ARTEMIS can reveal genome-wide repeat landscapes that reflect dramatic underlying changes in human cancers,” Annapragada says. “By illuminating the so-called ‘dark genome,’ the work offers unique insights into the cancer genome and provides a proof-of-concept for the utility of genome-wide repeat landscapes as tissue and blood-based biomarkers for cancer detection, characterization, and monitoring.” Next steps are to evaluate the approach in larger clinical trials, says Velculescu: “You can imagine this could be used for early detection for a variety of cancer types, but also could have uses in other applications such as monitoring response to treatment or detecting recurrence. This is a totally new frontier.” Reference: “Genome-wide repeat landscapes in cancer and cell-free DNA” by Akshaya V. Annapragada, Noushin Niknafs, James R. White, Daniel C. Bruhm, Christopher Cherry, Jamie E. Medina, Vilmos Adleff, Carolyn Hruban, Dimitrios Mathios, Zachariah H. Foda, Jillian Phallen, Robert B. Scharpf and Victor E. Velculescu, 13 March 2024, Science Translational Medicine. DOI: 10.1126/scitranslmed.adj9283 The work was supported in part by the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation, Stand Up to Cancer (SU2C) in-Time Lung Cancer Interception Dream Team Grant, SU2C-Dutch Cancer Society International Translational Cancer Research Dream Team Grant (SU2C-AACR-DT1415), the Gray Foundation, The Honorable Tina Brozman Foundation, the Commonwealth Foundation, the Mark Foundation for Cancer Research, the Cole Foundation, a research grant from Delfi Diagnostics and U.S. National Institutes of Health grants CA121113, CA006973, CA233259, CA062924, CA271896 and 1T32GM136577. Annapragada, Scharpf, and Velculescu are inventors on patent applications submitted by The Johns Hopkins University related to genome-wide repeat landscapes in cancer and cfDNA. Annapragada, Bruhm, Adleff, Mathios, Foda, Phallen and Scharpf are inventors on patent applications submitted by The Johns Hopkins University related to cell-free DNA for cancer detection that have been licensed to Delfi Diagnostics. White is the founder and owner of Resphera Biosciences LLC and serves as a consultant to Personal Genome Diagnostics Inc. and Delfi Diagnostics Inc. Cherry is the founder and owner of CMCC Consulting. Phallen, Adleff and Scharpf are founders of Delfi Diagnostics, and Adleff and Scharpf are consultants for this organization. Velculescu is a founder of Delfi Diagnostics, serves on the board of directors and owns Delfi Diagnostics stock, which is subject to certain restrictions under university policy. Additionally, The Johns Hopkins University owns equity in Delfi Diagnostics. Velculescu divested his equity in Personal Genome Diagnostics (PGDx) to LabCorp in February 2022. He is an inventor on patent applications submitted by The Johns Hopkins University related to cancer genomic analyses and cell-free DNA for cancer detection that have been licensed to one or more entities, including Delfi Diagnostics, LabCorp, Qiagen, Sysmex, Agios, Genzyme, Esoterix, Ventana and ManaT Bio. Under the terms of these license agreements, the university and inventors are entitled to fees and royalty distributions. Velculescu is also an adviser to Viron Therapeutics and Epitope. These arrangements have been reviewed and approved by The Johns Hopkins University in accordance with its conflict-of-interest policies.

UC San Diego research identifies critical metabolic pathways in early autism development, offering new avenues for early detection and pharmacological treatments. Findings suggest new possibilities for early autism detection. Researchers at the University of California San Diego School of Medicine have shed new light on the changes in metabolism that occur between birth and the presentation of autism spectrum disorder (ASD) later in childhood. The researchers discovered that a small number of biochemical pathways are responsible for the majority of these changes, which could help inform new early detection and prevention strategies for autism. “At birth, the physical appearance and behavior of a child who will develop autism over the next few years are indistinguishable from that of a neurotypical child. Indeed, in most cases the fate of the child with regard to autism is not set at birth,” said Robert Naviaux, M.D., Ph.D., professor in the Departments of Medicine, Pediatrics and Pathology at UC San Diego School of Medicine. “We’re starting to learn about the governing dynamics that regulate the transition from risk to the actual appearance of the first symptoms of ASD. Early diagnosis opens the possibility of early intervention and optimal outcomes.” Autism: A Complex Interplay of Factors ASD is a developmental disorder characterized by difficulties in socializing and communication, as well as repetitive and/or restrictive behaviors. For the majority of people with ASD, the condition is a significant disability, with only 10-20 percent of children diagnosed before 5 years of age able to live independently as adults. While autism is known to have strong genetic risk factors, there are also environmental risk factors that play a role in the development and severity of ASD. Naviaux and other researchers are discovering that the development of autism is governed by the real-time interaction of these varied factors. By studying the developmental biology of metabolism and how it differs in autism, new insights are emerging in ASD and other complex developmental disorders. “Behavior and metabolism are linked – you cannot separate them,” added Naviaux. To learn more about the early metabolic changes that occur in children with autism, researchers studied two cohorts of children. One cohort consisted of newborn children, in whom autism can’t be detected. The second cohort consisted of 5-year-old children, some of whom had been diagnosed with autism. When comparing the metabolic profiles of children in the cohort who were eventually diagnosed with autism to those who developed neurotypically, they found striking differences. Of the 50 different biochemical pathways the researchers investigated, just 14 were responsible for 80 percent of the metabolic impact of autism. New Insights Into Autism’s Biochemical Processes The pathways that were most changed are related to the cell danger response, a natural and universal cellular reaction to injury or metabolic stress. The body has biochemical safeguards in place that can shut down the cell danger response once the threat has passed, and Naviaux hypothesizes that autism occurs when these safeguards fail to develop normally. The result is heightened sensitivity to environmental stimuli, and this effect contributes to sensory sensitivities and other symptoms associated with autism. “Metabolism is the language that the brain, gut, and immune system use to communicate, and autism occurs when the communication between these systems is changed,” added Naviaux. The cell danger response is primarily regulated by adenosine triphosphate (ATP) the body’s chemical energy currency. While these ATP-signaling pathways do not develop normally in autism, they may be partially restorable with existing pharmaceutical drugs. In 2017, Naviaux and his team completed early clinical testing for suramin, the only drug approved in humans that can target ATP signaling and which is normally used to treat African sleeping sickness. Now, the researchers hope that by revealing the specific ATP-related pathways that are altered in autism, their work will help scientists develop more drugs that target these pathways to manage the symptoms of ASD. “Suramin is just one drug that targets the cell danger response,” he said. “Now that we’re closely interrogating how metabolism changes in ASD, we could be at the beginning of a drug renaissance that will create new options for treatment that never existed before.” Reference: “Metabolic network analysis of pre-ASD newborns and 5-year-old children with autism spectrum disorder” by Sai Sachin Lingampelly, Jane C. Naviaux, Luke S. Heuer, Jonathan M. Monk, Kefeng Li, Lin Wang, Lori Haapanen, Chelsea A. Kelland, Judy Van de Water and Robert K. Naviaux, 10 May 2024, Communications Biology. DOI: 10.1038/s42003-024-06102-y Co-authors on the study include: Sai Sachin Lingampelly, Jane C. Naviaux, Jonathan M. Monk, Kefeng Li and Lin Wang at UC San Diego School of Medicine and Luke S. Heuer, Lori Haapanen, Chelsea A. Kelland and Judy Van de Water at University of California Davis This work was funded, in part, by Autism Speaks (grant 7274), the National Center for Research Resources (grant UL1TR001442), and through various philanthropic gifts.

The Summit supercomputer revealed how damaged strands of DNA are surgically repaired by a molecular pathway called nucleotide excision repair, or NER. NER’s protein components can change shape to perform different functions of repair on broken strands of DNA (blue and red helix). Credit: Tanmoy Paul, Georgia State University Researchers harness the power of the world’s most advanced supercomputers to simulate the inner workings of cellular machinery that repairs DNA and helps prevent life-threatening diseases. Sunburn and premature aging are well-known consequences of exposure to ultraviolet (UV) radiation, tobacco smoke, and other carcinogens. But the damage goes beyond the surface – inside the body, these harmful agents can literally tear DNA apart. Understanding how the body repairs and protects itself from this DNA damage is crucial for advancing treatments for genetic disorders and life-threatening diseases like cancer. Yet, despite significant research and medical progress, many aspects of the molecular mechanisms behind DNA repair remain poorly understood. To shed light on this process, researchers at Georgia State University have spent the past several years leveraging the Summit supercomputer at the Department of Energy’s Oak Ridge National Laboratory. Their focus: a complex DNA repair mechanism known as nucleotide excision repair (NER). This pathway relies on a highly coordinated set of protein complexes that identify and remove damaged DNA with remarkable precision. In their latest study, published in Nature Communications, the team developed a detailed computer model of a key NER component known as the pre-incision complex (PInC). PInC plays a pivotal role in regulating DNA repair during the later stages of the NER pathway. By unraveling how PInC functions and fits into the broader repair sequence, researchers hope to uncover new therapeutic targets for treating cancer and preventing diseases associated with DNA damage and premature aging. “We’re interested in the way cells repair their genetic material,” said lead investigator Ivaylo Ivanov, a chemistry professor at Georgia State University. “NER is a versatile pathway that repairs all kinds of different DNA damage using a three-stage process that relies on delicately balanced molecular machinery. Unfortunately, harmful mutations can develop that interfere with this machinery and cause severe human diseases.” “Yet, the effects of genetic mutations can be strikingly different depending on their positions within the repair complexes. In some cases, mutations result in patients having UV light sensitivity and an extreme cancer predisposition. In other cases, they cause abnormal development and premature aging,” he said. “Why that happens is not completely understood at the molecular level. That’s the mystery our computer modeling efforts aim to unravel.” The three acts of repair NER unfolds in three distinct stages: recognition, verification, and repair. Each stage requires different groups of proteins to perform specific functions, much like a trauma team has different specialists needed to treat injured patients in the emergency room. In that way, the NER machinery can adapt and change its shape depending on the task at hand. In the first stage, the NER protein XPC (xeroderma pigmentosum group C) acts like a first responder that locates the site of the damaged DNA, or lesion, and then twists the DNA helix to make the damage accessible. XPC then calls in other repair proteins to help initiate the second stage, called damage verification, or lesion scanning. Here, the NER protein machinery shifts into its next shape. As XPC steps back, the protein complex called transcription factor IIH, or TFIIH (pronounced T-F-2-H), moves into position. TFIIH further unwinds the section of DNA and scans the newly exposed strand for lesions. After that, it’s in the hands of the surgeon — the PInC — in the third and final stage of repair. With the “patient” stabilized and prepped for surgery, the operation to remove the damaged DNA strand can begin. Two enzymes, XPF and XPG (xeroderma pigmentosum groups F and G), position themselves precisely on each side of the lesion and act as molecular scissors to cut out the damaged segment of DNA. Once the lesion is removed, new DNA is synthesized to fill in the gap left behind. Finally, the DNA backbone is sealed, and the damaged DNA is restored back to health. “What we want to know is how the PInC forms after the lesion scanning phase,” Ivanov said. “How does it control the positioning of the two enzyme subunits that perform the dual incision of the damaged DNA strand? And importantly, is there any cross talk between the two enzymes? Do they sense each other?” “That matters because once the damaged DNA strand is cleaved, it’s vital that the repair process is completed by filling in that gap,” he added. “Otherwise, it will lead to cell death or to the introduction of double-stranded breaks, which are extremely harmful to the cell.” Answering those questions required the researchers to solve the structure of the PInC. In biology, understanding protein structure is essential for understanding the behavior or function of protein assemblies. The shapes, sizes, and interactions of proteins determine how they fit together to form large biomolecular assemblies. “We integrated the structural model of PInC using data from a variety of biophysical techniques, notably cryo-electron microscopy,” Ivanov said. “But in the end, the computation is what puts everything together.” Much like the pieces of a jigsaw puzzle, the PInC model had to be assembled from known structures of constituent proteins, and all the individual pieces had to be put together in 3D. However, many of the PInC components had no known experimental structures. To overcome this challenge, the researchers used a neural network-based model called AlphaFold2 to predict the unknown structures and the interfaces between the proteins that hold PInC together. Summit’s final simulations “Computationally, once you assemble the PInC, molecular dynamics simulations of the complex become relatively straightforward, especially on large supercomputers like Summit,” Ivanov said. Nanoscale Molecular Dynamics, or NAMD, is a molecular dynamics code specifically designed for supercomputers and is used to simulate the movements and interactions of large biomolecular systems that contain millions of atoms. Using NAMD, the research team ran extensive simulations. The number-crunching power of the 200-petaflop Summit supercomputer — capable of performing 200,000 trillion calculations per second — was essential in unraveling the functional dynamics of the PInC complex on a timescale of microseconds. “The simulations showed us a lot about the complex nature of the PInC machinery. It showed us how these different components move together as modules and the subdivision of this complex into dynamic communities, which form the moving parts of this machine,” Ivanov said. The findings are significant in that mutations in XPF and XPG can lead to severe human genetic disorders. They include xeroderma pigmentosum, which is a condition that makes people more susceptible to skin cancer, and Cockayne syndrome, which can affect human growth and development, lead to impaired hearing and vision, and speed up the aging process. “Simulations allow us to zero in on these important regions because mutations that interfere with the function of the NER complex often occur at community interfaces, which are the most dynamic regions of the machine,” Ivanov said. “Now we have a much better understanding of how and from where these disorders manifest.” Most of the molecular dynamics simulations were performed on Summit. However, after 6 years of production, Summit was retired at the end of 2024. Looking ahead, Ivanov and his team plan to use Summit’s successor, Frontier, the exascale-class supercomputer that debuted as the world’s most powerful supercomputer when it came online in 2022. Their work on Frontier will involve examining transcription-coupled NER, which is a DNA repair process that fixes damage in actively transcribed genes to ensure that essential proteins can continue being made. Reference: “Dynamic conformational switching underlies TFIIH function in transcription and DNA repair and impacts genetic diseases” by Jina Yu, Chunli Yan, Thomas Dodd, Chi-Lin Tsai, John A. Tainer, Susan E. Tsutakawa and Ivaylo Ivanov, 13 May 2023, Nature Communications. DOI: 10.1038/s41467-023-38416-6 The study was funded by Advanced Scientific Computing Research.

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