bims-obesme Biomed News
on Obesity metabolism
Issue of 2025–05–25
seventeen papers selected by
Xiong Weng, University of Edinburgh
  1. Genetic underpinnnings of type 2 diabetes.
  2. Nicotinic acid riboside maintains NAD+ homeostasis and ameliorates aging-associated NAD+ decline.
  3. A liver-fat crosstalk for iron flux during healthy beiging of adipose tissue.
  4. Expanding the understanding of insulin resistance in brain and periphery.
  5. Targeting the chromatin remodeler BAZ2B mitigates hepatic senescence and MASH fibrosis.
  6. GLP-1R/GCGR dual agonism dissipates hepatic steatosis to restore insulin sensitivity and rescue pancreatic β-cell function in obese male mice.
  7. Mice lacking this amino acid lost 30% of their body weight.
  8. Adipocytes regulate monocyte development through the OGT-NEFA-CD36/FABP4 pathway in high-fat diet-induced obesity.
  9. Histone Lactylation Antagonizes Senescence and Skeletal Muscle Aging by Modulating Aging-Related Pathways.
  10. Enabling RNA-compatible synthetic receptors through RNA editing.
  11. Mitochondrial Bioenergetics in Physiology.
  12. Microbiome metabolism of dietary phytochemicals controls the anticancer activity of PI3K inhibitors.
  13. m6A modification is incorporated into bacterial mRNA without specific functional benefit.
  14. Clonal tracing with somatic epimutations reveals dynamics of blood ageing.
  15. De novo serine biosynthesis is protective in mitochondrial disease.
  16. From metabolomics to energy balance physiology.
  17. Comprehensive evaluation of phosphoproteomic-based kinase activity inference.
  1. Adv Genet. 2025 ;pii: S0065-2660(24)00040-3. [Epub ahead of print]113 54-75
    Genetic underpinnnings of type 2 diabetes.
    Aditya Shah, Clancy O Bush, Rachel J Perry.
      Genetics is a significant risk factor for developing type 2 diabetes, with a family history conferring a 1.5-3-fold increased risk. Intriguingly, this heritable risk is higher when the affected parent is the mother, suggesting a potential role of mitochondrial genetics -maternally inherited DNA - in diabetes pathogenesis, a hypothesis this chapter will explore. While obesity mediates some of the genetic risk of type 2 diabetes, the chapter and will focus on genetic influences on diabetes independent of obesity. Mechanistically, genetic variants directly or indirectly contribute to insulin resistance across key tissues, including liver, muscle and adipose tissue. This insulin resistance prevents the liver from efficiently suppressing glucose production in response to insulin and impairs glucose uptake in muscle during postprandial states. Insulin resistance is driven by complex interactions between the genome and environmental, which can, in turn, influence gene expression and contribute to worsening of metabolic dysfunction. This chapter examines how tissue-specific genetic changes drive insulin resistance in individual organs and how these localized dysfunctions contribute to the broader, multi-organ metabolic dysfunction that characterize type 2 diabetes.
    Keywords:  Adipose tissue; Beta cell; Liver; Mitochondrial uncoupling; Skeletal muscle; Type 2 diabetes
    DOI:  https://doi.org/10.1016/bs.adgen.2024.12.001
  2. Cell Metab. 2025 May 22. pii: S1550-4131(25)00260-8. [Epub ahead of print]
    Nicotinic acid riboside maintains NAD+ homeostasis and ameliorates aging-associated NAD+ decline.
    Won-Suk Song, Xiyu Shen, Kang Du, Cuauhtemoc B Ramirez, Sang Hee Park, Yang Cao, Johnny Le, Hosung Bae, Joohwan Kim, Yujin Chun, Nikki Joyce Khong, Marie Kim, Sunhee Jung, Wonsuk Choi, Miranda L Lopez, Zaid Said, Zehan Song, Sang-Guk Lee, Dequina Nicholas, Yo Sasaki, Jeffrey Milbrandt, David K Imagawa, Dorota Skowronska-Krawczyk, Danica Chen, Gina Lee, Cholsoon Jang, Qin Yang.
      
    DOI:  https://doi.org/10.1016/j.cmet.2025.05.004
  3. Autophagy Rep. 2024 ;3(1): 2396696
    A liver-fat crosstalk for iron flux during healthy beiging of adipose tissue.
    Jinying Yang, Limin Shi, Anna L Cubito, James F Collins, Zhiyong Cheng.
      Beiging of adipocytes is characteristic of a higher number of mitochondria, the central hub of metabolism in the cell. However, studies show that beiging can improve metabolic health or cause metabolic disorders. Here we discuss a liver-fat crosstalk for iron flux associated with healthy beiging of adipocytes. Deletion of the transcription factor FoxO1 in adipocytes (adO1KO mice) induces a higher iron flux from the liver to white adipose tissue, concurrent with augmented mitochondrial biogenesis that increases iron demands. In addition, adO1KO mice adopt an alternate mechanism to sustain mitophagy, which enhances mitochondrial quality control, thereby improving mitochondrial respiratory capacity and metabolic health. However, the liver-fat crosstalk is not detectable in adipose Atg7 knockout (ad7KO) mice, which undergo beiging of adipocytes but have metabolic dysregulation. Autophagic clearance of mitochondria is blocked in ad7KO mice, which accumulates dysfunctional mitochondria and elevates mitochondrial content but lowers mitochondrial respiratory capacity. Mitochondrial biogenesis is comparable in the control and ad7KO mice, and the iron influx into adipocytes and iron efflux from the liver remain unchanged. Therefore, activation of the liver-fat crosstalk is critical for mitochondrial quality control that underlies healthy beiging of adipocytes.
    Keywords:  Adipose beiging; Atg7; FoxO1; iron flux; liver-fat crosstalk
    DOI:  https://doi.org/10.1080/27694127.2024.2396696
  4. Trends Endocrinol Metab. 2025 May 19. pii: S1043-2760(25)00099-2. [Epub ahead of print]
    Expanding the understanding of insulin resistance in brain and periphery.
    Wenqiang Chen, Stephanie Kullmann, Elizabeth M Rhea.
      Insulin resistance is a central feature of metabolic disorders such as type 2 diabetes (T2D). While studies on this disorder have largely been linked to glucose metabolism and intracellular signaling, recent advances reveal that insulin resistance extends beyond traditional glucose regulatory pathways, impacting multiple organs including the brain, contributing to cognitive dysfunction and neurodegenerative diseases such as Alzheimer's disease (AD). This opinion revisits insulin resistance through molecular, cellular, and systemic perspectives, emphasizing the intersection between peripheral and brain insulin resistance (BIR), the role of the blood-brain barrier (BBB), and emerging biomarkers. Furthermore, we integrate insights from multi-omics and neuroimaging studies to refine our understanding, advocating for a broader perspective that informs early detection and intervention in metabolic and neurodegenerative diseases.
    Keywords:  insulin; insulin resistance; neurodegeneration; type 2 diabetes
    DOI:  https://doi.org/10.1016/j.tem.2025.04.010
  5. Nat Aging. 2025 May 19.
    Targeting the chromatin remodeler BAZ2B mitigates hepatic senescence and MASH fibrosis.
    Chuantao Tu, Cheng Qian, Shuyu Li, De-Ying Lin, Zhi-Yang Liu, Wan-Gan Ouyang, Xin-Lei Kang, Fangyuan Chen, Shu Song, Shi-Qing Cai.
      With increased age, the liver becomes more vulnerable to metabolic dysfunction-associated steatohepatitis (MASH) with fibrosis. Deciphering the complex interplay between aging, the emergence of senescent cells in the liver and MASH fibrosis is critical for developing treatments. Here we report an epigenetic mechanism that links liver aging to MASH fibrosis. We find that upregulation of the chromatin remodeler BAZ2B in a subpopulation of hepatocytes (HEPs) is linked to MASH pathology in patients. Genetic ablation or hepatocyte-specific knockdown of Baz2b in mice attenuates HEP senescence and MASH fibrosis by preserving peroxisome proliferator-activated receptor α (PPARα)-mediated lipid metabolism, which was impaired in both naturally aged and MASH mouse livers. Mechanistically, Baz2b downregulates the expression of genes related to the PPARα signaling pathway by directly binding their promoter regions and reducing chromatin accessibility. Thus, our study unravels the BAZ2B-PPARα-lipid metabolism axis as a link from liver aging to MASH fibrosis, suggesting that BAZ2B is a potential therapeutic target for HEP senescence and fibrosis.
    DOI:  https://doi.org/10.1038/s43587-025-00862-w
  6. Nat Commun. 2025 May 21. 16(1): 4714
    GLP-1R/GCGR dual agonism dissipates hepatic steatosis to restore insulin sensitivity and rescue pancreatic β-cell function in obese male mice.
    Rhianna C Laker, Shaun Egolf, Sarah Will, Louise Lantier, Owen P McGuinness, Charles Brown, Nicholas Bhagroo, Stephanie Oldham, Kyle Kuszpit, Alex Alfaro, Xidan Li, Taewook Kang, Giovanni Pellegrini, Anne-Christine Andréasson, Sarina Kajani, Sadichha Sitaula, Martin R Larsen, Christopher J Rhodes.
      An early driver of Type 2 diabetes mellitus (T2D) is ectopic fat accumulation, especially in the liver, that impairs insulin sensitivity. In T2D, GLP-1R/GCGR dual-agonists reduce glycaemia, body weight and hepatic steatosis. Here, we utilize cotadutide, a well characterized GLP-1R/GCGR dual-agonist, and demonstrate improvement of insulin sensitivity during hyperinsulinemic euglycemic clamp following sub-chronic dosing in male, diet-induced obese (DIO) mice. Phosphoproteomic analyses of insulin stimulated liver from cotadutide-treated mice identifies previously unknown and known phosphorylation sites on key insulin signaling proteins associated with improved insulin sensitivity. Cotadutide or GCGR mono-agonist treatment also increases brown adipose tissue (BAT) insulin-stimulated glucose uptake, while GLP-1R mono-agonist shows a weak effect. BAT from cotadutide-treated mice have induction of UCP-1 protein, increased mitochondrial area and a transcriptomic profile of increased fat oxidation and mitochondrial activity. Finally, the cotadutide-induced improvement in insulin sensitivity is associated with reduction of insulin secretion from isolated pancreatic islets indicating reduced insulin secretory demand. Here we show, GLP-1R/GCGR dual agonism provides multimodal efficacy to decrease hepatic steatosis and consequently improve insulin sensitivity, in concert with recovery of endogenous β-cell function and reduced insulin demand. This substantiates GLP-1R/GCGR dual-agonism as a potentially effective T2D treatment.
    DOI:  https://doi.org/10.1038/s41467-025-59773-4
  7. Nature. 2025 May 21.
    Mice lacking this amino acid lost 30% of their body weight.
    Rachel Fieldhouse.
      
    Keywords:  Diabetes; Metabolism; Obesity
    DOI:  https://doi.org/10.1038/d41586-025-01597-9
  8. Cell Death Dis. 2025 May 19. 16(1): 401
    Adipocytes regulate monocyte development through the OGT-NEFA-CD36/FABP4 pathway in high-fat diet-induced obesity.
    Na He, Yingjie Li, Fabao Liu, Xifeng Dong, Daoxin Ma.
      Obesity, resulting from excessive adipocyte accumulation, is a primary risk for various diseases. Although its impact on hematopoietic stem cell (HSC) function has been reported, its effects on HSC differentiation remain controversial. O-GlcNAc transferase (OGT), which catalyzes the attachment of N-acetylglucosamine to serine and threonine residues in proteins, acts as a metabolic sensor capable of regulating diverse physiological processes. This study demonstrates that obesity is associated with higher peripheral monocyte levels. Adipocyte OGT is crucial for monocyte development in high-fat diet (HFD)-induced obesity, promoting an increase in peripheral blood monocytes through transcriptional activation of nonesterified fatty acids (NEFA), a critical energy substrate. Loss of adipocyte OGT decreases serum NEFA levels, reduces white adipose tissue, and inhibits HSC differentiation into monocytes in HFD-induced obesity. Mechanistically, the regulated effect of adipocyte OGT on monocyte development may be mediated by NEFA-cluster of differentiation 36/fatty acid binding protein 4 (CD36/FABP4) pathway in HSCs in HFD-induced obesity. These findings establish the critical role of adipocyte OGT in hematopoietic homeostasis and monocyte development.
    DOI:  https://doi.org/10.1038/s41419-025-07721-x
  9. Adv Sci (Weinh). 2025 May 19. e2412747
    Histone Lactylation Antagonizes Senescence and Skeletal Muscle Aging by Modulating Aging-Related Pathways.
    Fanju Meng, Jianuo He, Xuebin Zhang, Wencong Lyu, Ran Wei, Shiyi Wang, Zhehao Du, Haochen Wang, Jinlong Bi, Xueyang Hua, Chao Zhang, Yiting Guan, Guoliang Lyu, Xiao-Li Tian, Lijun Zhang, Wenbing Xie, Wei Tao.
      Epigenetic alterations are among the prominent drivers of cellular senescence and/or aging, intricately orchestrating gene expression programs during these processes. This study shows that histone lactylation, plays a pivotal role in counteracting senescence and mitigating dysfunctions of skeletal muscle in aged mice. Mechanistically, histone lactylation and lactyl-CoA levels markedly decrease during cellular senescence but are restored under hypoxic conditions primarily due to elevated glycolytic activity. The enrichment of histone lactylation at promoters is essential for sustaining the expression of genes involved in the cell cycle and DNA repair pathways. Furthermore, the modulation of enzymes crucial for histone lactylation, leads to reduced histone lactylation and accelerated cellular senescence. Consistently, the suppression of glycolysis and the depletion of histone lactylation are also observed during skeletal muscle aging. Modulating the enzymes can also lead to the loss of histone lactylation in skeletal muscle, downregulating DNA repair and proteostasis pathways and accelerating muscle aging. Running exercise increases histone lactylation, which in turn upregulate key genes in the DNA repair and proteostasis pathways. This study highlights the significant roles of histone lactylation in modulating cellular senescence as well as muscle aging, providing a promising avenue for antiaging intervention via metabolic manipulation.
    Keywords:  epigenetics; histone lactylation; senescence; skeletal muscle aging
    DOI:  https://doi.org/10.1002/advs.202412747
  10. Nat Rev Mol Cell Biol. 2025 May 21.
    Enabling RNA-compatible synthetic receptors through RNA editing.
    Xiaowei Zhang, Luis S Mille-Fragoso.
      
    DOI:  https://doi.org/10.1038/s41580-025-00863-y
  11. Acta Physiol (Oxf). 2025 Jun;241(6): e70056
    Mitochondrial Bioenergetics in Physiology.
    Martin Jastroch, Michaela Keuper.
      
    Keywords:  bioenergetics; brown adipose tissue; disease; ectothermic; endothermic; mitochondria; sarcopenia; ucp1
    DOI:  https://doi.org/10.1111/apha.70056
  12. Cell. 2025 May 15. pii: S0092-8674(25)00511-2. [Epub ahead of print]
    Microbiome metabolism of dietary phytochemicals controls the anticancer activity of PI3K inhibitors.
    Asael Roichman, Qianying Zuo, Sunghoon Hwang, Wenyun Lu, Ricardo A Cordova, Michael R MacArthur, Jacob A Boyer, Sarah J Mitchell, Jesse Powers, Sophia A Koval, Craig J Hunter, Jamie Rijmers, Rolf-Peter Ryseck, Jenna E AbuSalim, Seema Chatterjee, Won Dong Lee, Xincheng Xu, Xi Xing, Zihong Chen, Xianfeng Zeng, Siddharth Marwaha, Matthew J McBride, Jessie Y Guo, Yibin Kang, Mohamed S Donia, Joshua D Rabinowitz.
      Phosphatidylinositol 3-kinase (PI3K) signaling is both the effector pathway of insulin and among the most frequently activated pathways in human cancer. In murine cancer models, the efficacy of PI3K inhibitors is dramatically enhanced by a ketogenic diet, with a proposed mechanism involving dietary suppression of insulin. Here, we confirm profound diet-PI3K anticancer synergy but show that it is, surprisingly, unrelated to diet macronutrient composition. Instead, the diet-PI3K interaction involves microbiome metabolism of ingested phytochemicals. Specifically, murine ketogenic diet lacks the complex spectrum of phytochemicals found in standard chow, including the soy phytochemicals soyasaponins. We find that soyasaponins are converted by the microbiome into inducers of hepatic cytochrome P450 enzymes, and thereby lower PI3K inhibitor blood levels and anticancer activity. A high-carbohydrate, low-phytochemical diet synergizes with PI3K inhibition to treat cancer in mice, as do antibiotics that curtail the gut microbiome. Thus, diet impacts anticancer drug activity through phytochemical-microbiome-liver interactions.
    Keywords:  PI3Ki; breast cancer; cytochrome P450; diet and cancer treatment; gut-liver axis; microbiome metabolites; pancreatic cancer; pharmacokinetics; phytochemicals; soyasaponins
    DOI:  https://doi.org/10.1016/j.cell.2025.04.041
  13. Nucleic Acids Res. 2025 May 22. pii: gkaf425. [Epub ahead of print]53(10):
    m6A modification is incorporated into bacterial mRNA without specific functional benefit.
    Klara Szydlo, Leonardo Santos, Thomas W Christian, Sunita Maharjan, Amir Dorsey, Isao Masuda, Jingxuan Jia, Yuan Wu, Weixin Tang, Ya-Ming Hou, Zoya Ignatova.
      N 6-Methyladenosine (m6A), the most abundant modification in eukaryotic messenger RNAs (mRNAs), has also been found at a low level in bacterial mRNAs. However, enzyme(s) that introduce m6A modification on mRNAs in bacteria remain elusive. In this work, we combine deep-sequencing approaches that identify m6A sites with in vitro biochemical studies to identify putative m6A methyltransferases that would modify Escherichia coli mRNAs. We tested four uncharacterized candidates predicted to encode proteins with putative methyltransferase domains, whose deletion decreased the m6A level. However, in vitro analysis with the purified putative methyltransferases revealed that none of them installs m6A on mRNA. Exposure to heat and oxidative stress also changed the m6A level; however, we found no clear correlation between the m6A change and the specific stress. Considering two deep-sequencing approaches with different resolution, we found that m6A methylation on bacterial mRNAs is very low and appears randomly introduced. These results suggest that, in contrast to eukaryotes, the m6A modification in bacterial mRNA lacks a direct enzymatic recognition mechanism and has no clear biological function.
    DOI:  https://doi.org/10.1093/nar/gkaf425
  14. Nature. 2025 May 21.
    Clonal tracing with somatic epimutations reveals dynamics of blood ageing.
    Michael Scherer, Indranil Singh, Martina Maria Braun, Chelsea Szu-Tu, Pedro Sanchez Sanchez, Dominik Lindenhofer, Niels Asger Jakobsen, Verena Körber, Michael Kardorff, Lena Nitsch, Pauline Kautz, Julia Rühle, Agostina Bianchi, Luca Cozzuto, Robert Frömel, Sergi Beneyto-Calabuig, Caleb Lareau, Ansuman T Satpathy, Renée Beekman, Lars M Steinmetz, Simon Raffel, Leif S Ludwig, Paresh Vyas, Alejo Rodriguez-Fraticelli, Lars Velten.
      Current approaches used to track stem cell clones through differentiation require genetic engineering1,2 or rely on sparse somatic DNA variants3,4, which limits their wide application. Here we discover that DNA methylation of a subset of CpG sites reflects cellular differentiation, whereas another subset undergoes stochastic epimutations and can serve as digital barcodes of clonal identity. We demonstrate that targeted single-cell profiling of DNA methylation5 at single-CpG resolution can accurately extract both layers of information. To that end, we develop EPI-Clone, a method for transgene-free lineage tracing at scale. Applied to mouse and human haematopoiesis, we capture hundreds of clonal differentiation trajectories across tens of individuals and 230,358 single cells. In mouse ageing, we demonstrate that myeloid bias and low output of old haematopoietic stem cells6 are restricted to a small number of expanded clones, whereas many functionally young-like clones persist in old age. In human ageing, clones with and without known driver mutations of clonal haematopoieis7 are part of a spectrum of age-related clonal expansions that display similar lineage biases. EPI-Clone enables accurate and transgene-free single-cell lineage tracing on hematopoietic cell state landscapes at scale.
    DOI:  https://doi.org/10.1038/s41586-025-09041-8
  15. Cell Rep. 2025 May 15. pii: S2211-1247(25)00481-4. [Epub ahead of print]44(5): 115710
    De novo serine biosynthesis is protective in mitochondrial disease.
    Christopher B Jackson, Anastasiia Marmyleva, Geoffray Monteuuis, Ryan Awadhpersad, Takayuki Mito, Nicola Zamboni, Takashi Tatsuta, Amy E Vincent, Liya Wang, Nahid A Khan, Thomas Langer, Christopher J Carroll, Anu Suomalainen.
      The importance of serine as a metabolic regulator is well known for tumors and is also gaining attention in degenerative diseases. Recent data indicate that de novo serine biosynthesis is an integral component of the metabolic response to mitochondrial disease, but the roles of the response have remained unknown. Here, we report that glucose-driven de novo serine biosynthesis maintains metabolic homeostasis in energetic stress. Pharmacological inhibition of the rate-limiting enzyme, phosphoglycerate dehydrogenase (PHGDH), aggravated mitochondrial muscle disease, suppressed oxidative phosphorylation and mitochondrial translation, altered whole-cell lipid profiles, and enhanced the mitochondrial integrated stress response (ISRmt) in vivo in skeletal muscle and in cultured cells. Our evidence indicates that de novo serine biosynthesis is essential to maintain mitochondrial respiration, redox balance, and cellular lipid homeostasis in skeletal muscle with mitochondrial dysfunction. Our evidence implies that interventions activating de novo serine synthesis may protect against mitochondrial failure in skeletal muscle.
    Keywords:  CP: Metabolism; de novo serine synthesis; mitochondrial disease; mitochondrial integrated stress response; mitochondrial translation; tissue specificity; treatment
    DOI:  https://doi.org/10.1016/j.celrep.2025.115710
  16. Adv Genet. 2025 ;pii: S0065-2660(24)00038-5. [Epub ahead of print]113 102-145
    From metabolomics to energy balance physiology.
    María José Ortuño Romero, Daxiang Na.
      Omics technologies are transforming our understanding of disease mechanisms and reshaping clinical practice. By enabling high-throughput, unbiased data collection at various molecular levels - including genes (genomics), mRNA (transcriptomics), proteins (proteomics), and metabolites (metabolomics) - omics approaches offer a comprehensive view of biological states in both health and disease. Among these, metabolomics has emerged as a pivotal tool, rapidly evolving beyond diagnostics to become a cutting-edge technique for pinpointing metabolites that regulate key physiological processes. This chapter reviews the advances in metabolomics, its integration with other omics approaches, and its applications, particularly emphasizing energy homeostasis. By incorporating metabolomic insights into physiology, we move closer to an integrative understanding of biological systems, laying the groundwork for novel therapies to combat obesity and related metabolic disorders.
    Keywords:  Lipidomics; Metabolomics; Obesity; Omics Integration
    DOI:  https://doi.org/10.1016/bs.adgen.2024.11.001
  17. Nat Commun. 2025 May 22. 16(1): 4771
    Comprehensive evaluation of phosphoproteomic-based kinase activity inference.
    Sophia Müller-Dott, Eric J Jaehnig, Khoi Pham Munchic, Wen Jiang, Tomer M Yaron-Barir, Sara R Savage, Martin Garrido-Rodriguez, Jared L Johnson, Alessandro Lussana, Evangelia Petsalaki, Jonathan T Lei, Aurelien Dugourd, Karsten Krug, Lewis C Cantley, D R Mani, Bing Zhang, Julio Saez-Rodriguez.
      Kinases regulate cellular processes and are essential for understanding cellular function and disease. To investigate the regulatory state of a kinase, numerous methods have been developed to infer kinase activities from phosphoproteomics data using kinase-substrate libraries. However, few phosphorylation sites can be attributed to an upstream kinase in these libraries, limiting the scope of kinase activity inference. Moreover, inferred activities vary across methods, necessitating evaluation for accurate interpretation. Here, we present benchmarKIN, an R package enabling comprehensive evaluation of kinase activity inference methods. Alongside classical perturbation experiments, benchmarKIN introduces a tumor-based benchmarking approach utilizing multi-omics data to identify highly active or inactive kinases. We used benchmarKIN to evaluate kinase-substrate libraries, inference algorithms and the potential of adding predicted kinase-substrate interactions to overcome the coverage limitations. Our evaluation shows most computational methods perform similarly, but the choice of library impacts the inferred activities with a combination of manually curated libraries demonstrating superior performance in recapitulating kinase activities. Additionally, in the tumor-based evaluation, adding predicted targets from NetworKIN further boosts the performance. We then demonstrate how kinase activity inference aids characterize kinase inhibitor responses in cell lines. Overall, benchmarKIN helps researchers to select reliable methods for identifying deregulated kinases.
    DOI:  https://doi.org/10.1038/s41467-025-59779-y
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