Biology subjects

Mueller, T.

Publications and source records attributed to Mueller, T..

At least 19 recordsLinked to original sources

bioRxiv2026

Targeting IGF2BP1 Creates a Mitotic Vulnerability in Colorectal Carcinoma

Background Mitotic dysregulation is a common feature of colorectal cancer (CRC), yet the contribution of post-transcriptional mechanisms remain incompletely understood. We investigated how the oncofetal RNA-binding protein IGF2BP1 supports mitotic integrity and exposes therapeutic vulnerabilities in CRC. Methods We integrated patient cohort analyses with genetic and pharmacological perturbation of IGF2BP1, transcriptomics, proteomics, RNA-binding assays and functional studies. Xenografts assessed tumor formation, while BTYNB-paclitaxel responses were examined in CRC cell lines and patient-derived organoids. Results IGF2BP1 expression was elevated in CRC, increased with tumor stage, and associated with poor survival and proliferative gene signatures. Genetic depletion or pharmacological inhibition of IGF2BP1 impaired cell viability, induced mitotic abnormalities, and promoted apoptosis, whereas its re-expression enhanced tumor formation in vivo. Integrated molecular analyses identified the chromosomal passenger complex (CPC) as a previously unrecognized downstream target of IGF2BP1. IGF2BP1 bound transcripts encoding CPC components and its depletion consistently reduced their expression across multiple cancer cell models. BTYNB disrupted IGF2BP1 association with INCENP, CDCA8, and BIRC5 transcripts and accelerated INCENP mRNA decay. Functionally, INCENP depletion recapitulated the mitotic defects and impaired viability observed upon IGF2BP1 inhibition. Exploiting this mitotic vulnerability, BTYNB synergized with paclitaxel in CRC cell lines and across four independent IGF2BP1-positive patient-derived organoid models. Conclusions Our findings uncover an IGF2BP1-dependent post-transcriptional regulatory mechanism sustaining CPC expression and mitotic integrity in CRC. Targeting this mechanism exposes a therapeutically exploitable mitotic vulnerability and provides a rationale for combining IGF2BP1 inhibition with microtubule-targeting agents.

cancer biology↗

bioRxiv2026

Two homologous Alt a1-like fungal proteins possess dual activities in HIR-associated immune signaling and EDS1-dependent cell death

Necrotrophic fungi secrete numerous Cell Death-Inducing Proteins (CDIPs) that manipulate host immunity to promote disease, yet the signaling pathways underlying their phytotoxic activity remain poorly understood. Here, we identify the Botrytis cinerea Hypersensitive response-inducing protein 1 (Hip1) as a close homolog of the recently described Sclerotinia sclerotiorum effector Plant Early Immunosuppressive Effector 1 (PEIE1) and investigate the molecular basis of its activity. HIP1 and PEIE1 share high sequence similarity and a conserved AlphaFold-predicted Alt a1-like fold, they interact with the Arabidopsis plasma membrane protein HIR4, and they induce strong necrosis in Nicotiana benthamiana. Despite their high structural similarity, Hip1 and PEIE1 differ in their reported roles during fungal infection. Unexpectedly, Hip1-induced cell death requires the central immune regulator ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1) as well as the downstream helper NLR network comprising ADR1 and NRG1. Together, our findings establish Hip1 as a closely related homolog of PEIE1 and suggest that these closely related Alt a1-like proteins possess dual activities: modulation of HIR-associated immune signaling and activation of EDS1-dependent host cell death.

plant biology↗

bioRxiv2026

Side-necked turtle genomes reveal chromosomal dynamics, skeletal innovation and cancer resistance

Turtles exhibit a highly derived body plan, exceptional longevity, cancer resistance, and striking diversity in karyotypes and sex determination systems. However, the genomic basis of these innovations remains unresolved, largely because reference genomes were lacking for one of two extant turtle clades, the side-necked turtles (Pleurodira). As part of the Vertebrate Genomes Project, we generated seven reference-quality Pleurodira genomes and reconstructed the most comprehensive genome-wide turtle phylogeny. Combining demographic inference with historical climate and biome reconstructions indicates that ancient climate fluctuations shaped long-term population dynamics, while recent declines mainly reflect population structure. Ancestral genome reconstructions reveal that rare bursts of chromosome fusions and fissions, likely facilitated by repetitive elements, drove turtle karyotype diversity. By identifying sex chromosomes and tracing their evolutionary history, we resolve a long-standing debate and demonstrate a single origin of genetic sex determination in Chelidae on a microchromosome over 80 million years ago. Contrary to previous hypotheses, we find no evidence of coevolution between genetic sex determination and chromosome number in turtles. Comparative genomic analyses further identify gene losses and signatures of adaptive evolution associated with key turtle traits. Gene losses causing disproportionate dwarfism phenotypes may have contributed to skeletal adaptations underlying the compact turtle body plan. In addition, gene losses and adaptive changes in stress response and tumor suppressor pathways likely enhance oxidative stress tolerance and cancer resistance. Together, these findings illuminate turtle genome evolution, revealing chromosomal dynamics, sex chromosome evolution, molecular insights into skeletal innovation and cancer resistance, and implicate gene losses as a recurrent contributor to evolutionary novelty.

genomics↗

bioRxiv2025

Gas5A, a putative glucanosyltransferase from Botrytis, functions as cell death inducing protein in plants

The necrotrophic fungus Botrytis cinerea, releases numerous phytotoxic, cell death inducing proteins (CDIPs) during infection. The precise role of these proteins and their molecular function, however, is still unknown. Here, we report on the identification of a previously unknown CDIP, the glucanosyltransferase Gas5A. Functional characterization revealed that the C-terminal 60 aa of Gas5A are sufficient to induce cell death, independent from its putative enzymatic function. Gas5A localization and functional dependence on the receptor-associated kinase suppressor of BIR1-1 (SOBIR1) and the plant defense regulator ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1) indicate recognition as a pathogen-associated molecular pattern (PAMP) at the plant plasma membrane, but it is toxic also when delivered inside plant cells. Generation of a CRISPR/Cas9-assisted Botrytis knockout strain did not indicate any impact of Gas5A on virulence. Taken together, Gas5A represents a novel PAMP-like CDIP with additional intracellular phytotoxic activity.

plant biology↗

bioRxiv2025

The Ca2+-binding protein CSE links Ca2+-signaling with cell-cell communication in multicellular cyanobacteria

Abstract/SummaryBecause of their multicellular lifestyle, filamentous cyanobacteria have evolved sophisticated cell-cell communication machinery to exchange, synchronize, and coordinate the efforts of individual cells in the filament. Analogous to gap junctions that were regarded as a purely Eukaryotic feature, multicellular cyanobacteria were found also to coordinate their cell-cell communication via septal junctions (SJs). However, the molecular signals that regulate the cell-cell communication machinery and SJs assembly are largely unknown. Lately, Ca2+- signaling has been implicated in regulating cell junctions in neurons. We recently discovered a new Ca2+-sensor protein, CSE, exclusively found in multicellular cyanobacteria. Here, we investigated CSE as a potential link between intracellular Ca2+-signaling and cell-cell communication. We solved the solution NMR structure of CSE in its Ca2+-bound state and revealed that CSE acts as Ca2+-buffer protein. Using cryo-electron tomography, we showed that CSE is not only essential for Ca2+ homeostasis, but also mediates cell-cell communication via regulating the formation of nanopores -- a necessary precursor of SJs -- as {Delta}cse mutant shows a strong reduction in the number of both nanopores and SJs. This determines for the first time Ca2+-signaling as a novel mechanism controlling cell-cell communication and establishes CSE as a key player regulating cyanobacterial multicellularity. This highlights also Ca2+-signaling as a common conserved principle for regulating cell junctions between organisms that deviated billion years ago.

microbiology↗

bioRxiv2025

MoveTraits - A database for integrating animal behaviour into trait-based ecology

Trait-based approaches are key to understanding eco-evolutionary processes but rarely account for animal behaviour despite its central role in ecosystem dynamics. We propose integrating behaviour into trait-based ecology through movement traits - standardised and comparable measures of animal movement derived from biologging data, such as daily displacements or range sizes. Accounting for animal behaviour will advance trait-based research on species interactions, community structure, and ecosystem functioning. Importantly, movement traits allow for quantification of behavioural reaction norms, offering insights into species acclimation and adaptive capacity to environmental change. We outline a vision for a living global movement trait database that enhances trait data curation by (1) continuously growing alongside shared biologging data, (2) calculating traits directly from individual-level data using standardised, consistent methodology, and (3) providing information on multi-level (species, individual, within-individual) trait variation. We present a proof-of-concept MoveTraits database with 55 mammal and 108 bird species, demonstrating calculation workflows for 5 traits across multiple time scales. Movement traits have significant potential to improve trait-based global change predictions and contribute to global biodiversity assessments as Essential Biodiversity Variables. By making animal movement data more accessible and interpretable, this database could bridge the gap between movement ecology and biodiversity policy, facilitating evidence-based conservation.

ecology↗

bioRxiv2025

A century-old museum sample reveals abandavirus with modern day presence in northernEuropean bats

Ancient genome sequences provide invaluable insights into the origin and evolution of viral pathogens, offering a broader temporal perspective that extends well beyond the limited timespan of clinical data, which typically covers at most a few decades. Whereas ancient viral DNA is relatively frequently recovered, ancient viral RNA genomes are scarce due to the fragile nature of RNA molecules. In this study, we explored the feasibility of detecting ancient viral RNA in ethanol-preserved bat samples from a museum collection. We not only detected viral genome fragments but also recovered the coding-complete genome of a bandavirus (species Bandavirus zwieselense, family Phenuiviridae, order Hareavirales, class Bunyaviricetes) from a Common pipistrelle (Pipistrellus pipistrellus) bat collected in northern Germany in 1919. To investigate the modern distribution of Bandavirus zwieselense, we screened bat organs collected in Germany and the Netherlands via RT-qPCR, identifying modern counterparts in nine Common Pipistrelle (P. pipistrellus) bats (collected between 2010 and 2018), and one Serotine bat (Eptesicus serotinus, collected in 1999). The resulting genomic data enabled us to map phylogenetic relationships within this previously uncharacterized virus species (Bandavirus zwieselense) and estimate the timeframe for the most recent common ancestor. Additionally, we performed functional analysis of the S segment encoded nonstructural (NSs) protein of Bandavirus zwieselense in human HEK-293T cells, demonstrating its ability to block interferon induction, a characteristic also observed in the related human-pathogenic Severe fever with thrombocytopenia syndrome virus (SFTSV, species Bandavirus dabieense). This study demonstrates the feasibility of recovering and characterizing viral genomes from ethanol-preserved ancient RNA material, underscoring the significant potential of museum collections to contribute to the understanding of RNA virus evolution.

microbiology↗

bioRxiv2025

Analysis of lhx8a, isl1, pax6a/b, calb2a and sst7 Reveals that Dopaminergic Neurons in the Zebrafish Subpallium Belong to the Extended Amygdala

The amygdala is a heterogenous multinuclear telencephalic structure critical for motivated and emotion-related behaviors in vertebrates. In ray-finned fish (actinopterygii) like the teleost zebrafish, a telencephalic outward growing process called eversion makes defining amygdaloid territories particularly challenging. Teleosts are also peculiar in that they develop prominent dopaminergic neuron groups in the subpallium, which are absent from tetrapods. To shed light on amygdala organization in teleosts, we pursued an evolutionary-developmental approach focusing on the topological origin of subpallial dopaminergic neurons. Specifically, we analyzed developmental expression patterns of Tyrosine hydroxylase in conjunction with pax6a+b, isl1a, nkx2.1, lhx8a, calb2a as telencephalic topology markers in brains of 5- and 30-day-old zebrafish (Danio rerio, Teleostei). Our results reveal, that the subpallial dopaminergic neurons develop within a pax6a negative dorsal subpallial domain (Vdd), which forms a primordial portion of the extended amygdala, including the medial amygdala and the anterior bed nucleus of the stria terminalis. Moreover, these dopaminergic neurons differentially coexpress calb2a and sst7, indicating population heterogeneity and potentially functional diversity. Our data also show that the zebrafish extended amygdala is formed by the dorsal LGE-like Vdd, which is subdivided into a Vdd2 subdivision that may correspond to the extended medial amygdala, including the bed nucleus of the stria terminalis, and forms the pallial-subpallial border region, and a more ventral Vdd1 that is pax6a positive and that corresponds to the central amygdala. Our work contributes to understanding development and evolution of the amygdala, and provides a foundation for functional analysis of the newly defined dopaminergic subtypes of the extended amygdala.

neuroscience↗

bioRxiv2024

Assessment of neurobehavioural traits under axenic conditions: an approach for multiple longitudinal analyses in the same mouse.

The gut-microbiota-brain axis influences neuroinflammation, neural development and behaviour such as sociability, memory and anxiety. To study these traits in vivo, especially during development or disease, it is crucial to analyse them over time and with multiple analyses in the same animal. With a growing understanding of the role of specific bacteria in neurodegenerative disease and behaviour, the demand for gnotobiotic mouse models has increased. However, maintaining stable hygienic conditions during behavioural testing is challenging, as exposure to conventional environments can alter the hygienic status of mice and affect behaviour. We established protocols to perform behavioural tests assessing memory, anxiety, exploration, learning and recognition under axenic conditions using flexible film isolators. Our study compared the behaviour of germ-free mice with mice carrying a defined minimal or moderately diverse microbiota. The results showed no effect of the microbiota on short- and long-term memory or novel object recognition. However, we showed for the first time that mice colonised with defined commensal bacteria exhibited more anxiety-like behaviour than germ-free mice. In addition, we showed that microbiota complexity is important, as only mice colonised with moderately diverse microbiota exhibited anxiety-like behaviour, allowing us to disentangle the contribution of specific microbial species or community interactions to this phenotype. This phenotype correlated with differences in hippocampal and serum metabolic profiles between colonised and germ-free mice. We propose a novel approach to study rodent behaviour at different physiological and pathological stages in their life without compromising hygiene, thus promoting the refinement and reduction of mice used in experiments.

animal behavior and cognition↗

bioRxiv2024

Alpha-synuclein preformed fibril-induced aggregation and dopaminergic cell death in cathepsin D overexpression and ZKSCAN3 knockout mice

-synuclein accumulation is recognized as a prominent feature in the majority of Parkinsons disease cases and also occurs in a broad range of neurodegenerative disorders including Alzheimers disease. It has been shown that -synuclein can spread from a donor cell to neighboring cells and thus propagate cellular damage, antagonizing the effectiveness of therapies such as transplantation of fetal or iPSC derived dopaminergic cells. As we and others previously have shown, insufficient lysosomal function due to genetic mutations or targeted disruption of cathepsin D can cause -synuclein accumulation. We here investigated whether overexpression of cathepsin D or knockout (KO) of the transcriptional suppressor of lysosomal biogenesis ZKSCAN3 can attenuate propagation of -synuclein aggregation and cell death. We examined dopaminergic neurodegeneration in the substantia nigra using stereology of tyrosine hydroxylase-immunoreactive cells 4 months and 6 months after intrastriatal injection of -synuclein preformed fibrils or monomeric -synuclein control in control, central nervous system (CNS)-cathepsin D overexpressing and CNS-specific ZKSCAN3 KO mice. We also examined pS129--synuclein aggregates in the substantia nigra, cortex, amygdala and striatum. The extent of dopaminergic neurodegeneration and pS129--synuclein aggregation in the brains of CNS-specific ZKSCAN3 knockout mice and CNS-cathepsin D overexpressing mice was similar to that observed in wild-type mice. Our results indicate that neither enhancing cathepsin D expression nor disrupting ZKSCAN3 in the CNS is sufficient to attenuate pS129--synuclein aggregate accumulation or dopaminergic neurodegeneration.

neuroscience↗

bioRxiv2024

The lincRNA Pantr1 is a FOXG1 target gene conferring site-specific chromatin binding of FOXG1

Derailed gene expression programs within the developing nervous system, encompassing both transcriptional and posttranscriptional processes, can cause diverse neurodevelopmental diseases (NDD). The NDD FOXG1-syndrome lacks full understanding of the mechanistic role of its eponymous gene product. While it is known that FOXG1 acts in part at the chromatin by binding to regulative regions, it is unclear what factors control its presence at specific sites. Long non-coding RNAs (lncRNAs) can mediate site-directed transcription factor binding, but their potential role in FOXG1-syndrome has not been described. Here, we show that FOXG1 localisation is regulated at selected loci through the lncRNA Pantr1. We identified FOXG1 as an upstream transcriptional activator of Pantr1 in human and mice. Further, we discovered that FOXG1 has the ability to associate with RNAs. Both, transcriptional regulation of Pantr1 by FOXG1 and association of both partners, build up a regulative network that impacts the localisation of FOXG1 at selected genomic loci. Specifically, Pantr1 facilitates cooperative presence of FOXG1/NEUROD1 at specific sites, and Pantr1 reduction leads to redistribution of FOXG1 to comparably more generic binding sites. The rescue of impaired dendritic outgrowth upon FOXG1 reduction by simultaneous overexpression of Pantr1 underlines the importance of the FOXG1/Pantr1 regulative network. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=79 SRC="FIGDIR/small/610239v1_ufig1.gif" ALT="Figure 1"> View larger version (23K): org.highwire.dtl.DTLVardef@19ecb05org.highwire.dtl.DTLVardef@22cfbcorg.highwire.dtl.DTLVardef@1748056org.highwire.dtl.DTLVardef@1959e3c_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2024

A deep-learning based analysis framework for ultra-high throughput screening time-series data

Analysis of ultra-high-throughput screening data sets is a highly critical step in drug discovery campaigns. Due to various environmental and experimental error sources fast and reliable identification of possible candidate compounds is challenging. In this work, we introduce a novel deep-learning based analysis framework to analyze uHTS time-series data sets. Our framework is based on two independent deep-learning models. A deep-learning regression model reduces temporal and spatial signal variation across multitier plates caused by systematic and random errors and a separate variational autoencoder model is used for dimensionality reduction. In contrast to classical evaluation methods our approach is capable to derive lower dimensional representations of time-series signals without a-priori knowledge of the data generating mechanism. We tested our analysis framework on an experimental uHTS data set and identified two distinct classes of substances in the screened library which could be attributed to two biological modes of action. Selected substances belonging to both modes of action were successfully validated in a secondary screening experiment.

bioinformatics↗

bioRxiv2024

APOE4 increases energy metabolism in APOE-isogenic iPSC-derived neurons

The apolipoprotein E4 (APOE4) allele represents the major genetic risk factor for Alzheimers disease (AD). In contrast, APOE2 is known to lower the AD risk while APOE3 is defined as risk neutral. APOE plays a prominent role in the bioenergetic homeostasis of the brain, and early-stage metabolic changes have been detected in brains of AD patients. Although APOE is primarily expressed by astrocytes in the brain, neurons also have been shown as source for APOE. However, little is known about the differential role of the three APOE isoforms for neuronal energy homeostasis. In this study, we generated pure human neurons (iN cells) from APOE-isogenic induced pluripotent stem cells (iPSCs), expressing either APOE2, APOE3, APOE4 or carrying an APOE-knockout (KO) to investigate APOE isoform-specific effects on neuronal energy metabolism. We showed that endogenously produced APOE4 enhanced mitochondrial ATP production in APOE-isogenic iN cells but not in the corresponding iPS cell line. This effect neither correlated with the expression levels of mitochondrial fission or fusion proteins, nor with the intracellular or secreted levels of APOE, which were similar for APOE2, APOE3 and APOE4 iN cells. ATP production and basal respiration in APOE-KO iN cells strongly differed from APOE4 and more closely resembled APOE2 and APOE3 iN cells indicating a gain-of-function mechanism of APOE4 rather than a loss-of-function. Taken together, our findings in APOE isogenic iN cells reveal an APOE genotype-dependent and neuron-specific regulation of oxidative energy metabolism.

neuroscience↗

bioRxiv2024

High-throughput proteome profiling with low variation in a multi-center study using dia-PASEF

High throughput proteomics is gaining increasing traction as it facilitates screening of large sample cohorts required in clinical research and systems biology studies. Recent developments in mass spectrometry-based proteomics resulted in improved hardware and software providing deep proteome coverage, robustness, and scale accessible to a wide range of laboratories. Here, we benchmark dia-PASEF, a data-independent acquisition scheme that integrates trapped ion mobility with high scan speed, with a high-resolution time-of-flight mass analyzer (timsTOF HT) for the deep proteome analysis of a human cell line applying short 5-minute gradients. To show intra-and interlaboratory reproducibility, we performed a multi-laboratory study including 11 sites. We demonstrate that on average 7,072 protein groups and 99,835 peptides were identified in human chronic myelogenous leukemia cells on the timsTOF HT with low variation. Our results underline that dia-PASEF data acquisition combined with reproducible chromatography enables high robustness and data consistency across instruments and laboratories, which is a prerequisite for translational biomedical insights.

systems biology↗

bioRxiv2024

ThirdPeak: A flexible tool designed for the robust analysis of two- and three-dimensional (single-molecule) tracking data.

ThirdPeak is an open-source tool tailored for the comprehensive analysis of two- and three-dimensional track data across various scales. Its versatile import options facilitate seamless integration into established workflows, and the user interface allows for swift visualization and analysis of the data. When applied to live-cell diffusion data, this software unveils the advantages of combining both 2D and 3D analysis, providing valuable insights into the understanding of biological processes.

biophysics↗

bioRxiv2023

Plant infection by the necrotrophic fungus Botrytis requires actin-dependent generation of high invasive turgor pressure

The devastating pathogen Botrytis cinerea infects a broad spectrum of host plants, causing great socio-economic losses. The necrotrophic fungus rapidly kills plant cells, nourishing their walls and cellular contents. To this end, necrotrophs secretes a cocktail of cell wall degrading enzymes, phytotoxic proteins and metabolites. Additionally, many fungi produce specialized invasion organs that generate high invasive pressures to force their way into the plant cell. However, for most necrotrophs, including Botrytis, the biomechanics of penetration and its contribution to virulence are poorly understood. Here we use a combination of quantitative micromechanical imaging and CRISPR-Cas guided mutagenesis to show that Botrytis uses substantial invasive pressure, in combination with strong surface adherence, for penetration. We found that the fungus establishes a unique mechanical geometry of penetration that develops over time during penetration events, and which is actin cytoskeleton dependent. Furthermore, interference of force generation by blocking actin polymerization was found to decrease Botrytis virulence, indicating that also for necrotrophs, mechanical pressure is important in host colonization. Our results demonstrate for the first time mechanistically how a necrotrophic fungus such as Botrytis employs this "brute force" approach, in addition to the secretion of lytic proteins and phytotoxic metabolites, to overcome plant host resistance.

biophysics↗

bioRxiv2023

The second messenger c-di-AMP controls natural competence via ComFB signaling protein

Natural competence requires a contractile pilus system. Here, we provide evidence that the pilus biogenesis and natural competence in cyanobacteria are regulated by the second messenger c-di-AMP. Furthermore, we show that the ComFB signaling protein is a novel c-di-AMP-receptor protein, widespread in bacterial phyla, and required for pilus biogenesis and DNA uptake.

microbiology↗

bioRxiv2023

A single-sample workflow for joint metabolomic and proteomic analysis of clinical specimens

Understanding the interplay of the proteome and the metabolome aids in understanding cellular phenotypes. To enable more robust inferences from such multi-omics analyses, combining proteomic and metabolomic datasets from the same sample provides major benefits by reducing technical variation between extracts during the pre-analytical phase, decreasing sample variation due to varying cellular content between aliquots, and limiting the required sample amount. We evaluated the advantages, practicality and feasibility of a single-sample workflow for combined proteome and metabolome analysis. In the workflow, termed MTBE-SP3, we combined a fully automated protein lysis and extraction protocol (autoSP3) with a semi-automated biphasic 75% EtOH/MTBE extraction for quantification of polar/non-polar metabolites. Additionally, we compared the resulting proteome of various biological matrices (FFPE tissue, fresh-frozen tissue, plasma, serum and cells) between autoSP3 and MTBE-SP3. Our analysis revealed that the single-sample workflow provided similar results to those obtained from autoSP3 alone, with an 85-98% overlap of proteins detected across the different biological matrices. Additionally, it provides distinct advantages by decreasing (tissue) heterogeneity by retrieving metabolomics and proteomic data from the identical biological material, and limiting the total amount of required material. Lastly, we applied MTBE-SP3 to a lung adenocarcinoma cohort of 10 patients. Integrating the metabolic and proteomic alterations between tumour and non-tumour adjacent tissue yielded consistent data independent of the method used. This revealed mitochondrial dysfunction in tumor tissue through deregulation of OGDH, SDH family enzymes and PKM. In summary, MTBE-SP3 enables the facile and confident parallel measurement of proteins and metabolites obtained from the same sample. This workflow is particularly applicable for studies with limited sample availability and offers the potential to enhance the integration of metabolomic and proteomic datasets.

cancer biology↗