Biology subjects

Lee, H.

Publications and source records attributed to Lee, H..

At least 19 recordsLinked to original sources

bioRxiv2026

Disrupted RGS coupling underlies a clinically distinct subset of GNAO1-related disorder

Heterotrimeric G proteins are transducers for a wide variety of neurotransmitter receptors. Mutations in the G protein o subunit are implicated in an early-onset neurological condition, GNAO1-related disorder, that manifests as movement disorders, developmental delays, and/or epileptic seizures. In a screen of disease-linked mutations in Go, we identified a subset that had no obvious biochemical defects, warranting further investigation. By structural modeling, protein-protein binding experiments in vitro and in cells, as well as measures of downstream ion channel electrophysiology, we identified a subset that impairs interactions with regulator of G protein signaling (RGS) proteins. RGS proteins accelerate G protein GTPase activity and are therefore critical for proper neurotransmitter signaling. Further, synthesis of current clinical data revealed that patients harboring these variants have comparatively mild symptoms. Our study demonstrates the importance of RGS regulation in G protein function, cell signaling, and human neurobiology.

biochemistry↗

bioRxiv2026

ssDNA hand-off from RPA to Polθ drives microhomology-mediated end-joining

DNA polymerase theta-mediated end joining (TMEJ) is the primary mechanism of double strand break repair in mitosis and becomes essential in BRCA-deficient cells. RPA, the ssDNA-binding protein that coats resected DNA ends, has long been thought to inhibit this pathway by blocking the initial microhomology search in TMEJ. Here we find instead that RPA plays an essential activating role in TMEJ. Structural, biochemical, and genetic analyses support a model in which Pol{theta} binds directly to RPA at resected DNA ends and then competes with RPA for ssDNA. This releases ssDNA into the Pol{theta} helicase domain. We propose that threading two DNA ends through the Pol{theta} dimer in this manner initiates the search for microhomology. Together, our findings establish a detailed mechanism of how proteins can harness RPA to access ssDNA for critical genome maintenance transactions.

biochemistry↗

bioRxiv2026

Glycogen removal enhances ethylene production in Synechocystis sp. PCC 6803 but exposes a 2-oxoglutarate-GS-GOGAT-phosphate constraint

Cyanobacteria are promising platforms for converting CO2 directly into value-added chemicals. However, redirecting fixed carbon toward a product requires understanding of how cells balance the energetic and redox supplies and demands - and how efficiently metabolic flux can be channelled into product formation rather than being dissipated or excreted. Glycogen, synthesized via ADP-glucose pyrophosphorylase (GlgC), is the major native carbon and energy sink, and its removal forces cells to redirect excess carbon and reducing power into alternative pathways. As a target product we used ethylene, a major industrial building block currently derived almost entirely from fossil feedstocks, which can be produced photoautotrophically by the ethylene-forming enzyme (EFE) at the expense of 2-oxoglutarate (2-OG), a central node linking carbon and nitrogen metabolism. Here, we compared wild-type Synechocystis sp. PCC 6803 with strains carrying either a complete ({Delta}glgC) or attenuated, light-responsive (LGS; psbA2-driven glgC) glycogen synthesis block, with an EFE-expressing strain (EFE), and with the combined {Delta}glgC+EFE strain. All strains were cultivated across a light gradient (35-300 mol photons m-2 s-1) under nitrogen-replete conditions. Integrating measurements of growth and ethylene production rates, chlorophyll-fluorescence analysis, quantitative proteomics, FTIR profiling, and overflow-metabolite analysis revealed that partial suppression of glycogen synthesis (LGS) enhanced growth under low irradiance but became detrimental above a critical light threshold. EFE expression in the {Delta}glgC background increased ethylene production in a light-dependent manner but further compromised growth. Both strains with EFE increased photosynthetic electron transport consistent with the carbon-sink effect, yet this electron surplus was not channelled proportionally into product or biomass. Instead, continuous 2-OG drain by EFE constrained flux through the GS-GOGAT node and induced a secondary inorganic phosphate limitation in {Delta}glgC+EFE that activated photoprotection and limited productivity. These results point to the 2-OG/GS-GOGAT/Pi axis as a key design constraint determining whether the surplus photosynthetic flux gets converted into product, dissipated through photoprotection, or released as overflow metabolites.

plant biology↗

bioRxiv2026

Macrophage-Derived 25-Hydroxycholesterol Drives Statin-Associated Acute Kidney Injury

Although acute kidney injury (AKI) has been implicated as a potential adverse effect of statin therapy, experimental evidence supporting this association remains limited. Here, we investigated whether elevated levels of 25-hydroxycholesterol (25-HC), an oxysterol produced by activated macrophages and monocytes, increase susceptibility to statin-induced AKI. We found that atorvastatin and fluvastatin induced cell death in proximal tubular cells when combined with 25-HC. Consistently, administration of low-dose lipopolysaccharide triggered AKI in statin-treated mice. Mechanistically, impaired protein prenylation disrupted the autophagosome-lysosome pathway in proximal tubular cells. AKI was attenuated by mevalonate supplementation, which restored protein prenylation, and by macrophage/monocyte depletion, which reduced the cellular sources of 25-HC. Furthermore, combined exposure to fluvastatin and 25-HC increased kidney injury molecule-1 (KIM-1) expression in human induced pluripotent stem cell-derived kidney organoids. Together, these findings suggest that elevated macrophage-derived 25-HC under conditions of infection, inflammation, or major surgery may increase susceptibility to statin-induced AKI. Our study identifies a previously unrecognized interaction between statins and 25-HC and suggests potential strategies to mitigate kidney injury while preserving the therapeutic benefits of statins.

pharmacology and toxicology↗

bioRxiv2026

Brainstem premotor circuits transform dental sensory input into coordinated jaw opening

Protective actions require the rapid transformation of damage into coordinated activity of motor pools, yet the brainstem circuits implementing this operation remain poorly defined. Here, we use the tooth-trigeminal system to identify molecularly specified pathways linking intradental sensory input to opposing jaw motor pools. Optogenetic activation of tooth-associated sensory afferents evoked rapid, stimulus-locked jaw-opening. Intradental afferents formed functional monosynaptic connections with Pdyn+ neurons in the 5Sol transition zone and Calb2+ neurons in the 5Tr transition zone, identifying these regions as sensory-recipient premotor interfaces. Predominantly excitatory Pdyn+ 5Sol neurons provided monosynaptic input to anterior digastric motor neurons, whereas predominantly inhibitory Calb2+ 5Tr neurons provided bilateral monosynaptic input to masseter motor neurons. Activation of Pdyn+ 5Sol neurons was sufficient to evoke jaw opening. Together, these findings define complementary brainstem pathways positioned to couple jaw-opening drive with inhibition of antagonistic jaw-closing output, revealing a withdrawal-like sensorimotor computation adapted to cranial biomechanics.

neuroscience↗

bioRxiv2026

A rapid, genetically-tractable human iPSC-derived model for studying tissue-resident macrophage biology in Alzheimer's and other diseases

Large-scale genetic and preclinical studies strongly implicate myeloid cells, particularly brain-resident macrophages, in the pathogenesis of Alzheimer's disease (AD). Efferocytic clearance of apoptotic cells and other cholesterol-rich cellular debris is a core macrophage function and represents an active area of AD research. However, human tissue-resident macrophages remain difficult to model in vitro as they acquire their transcriptional and functional identities in response to signals from their host tissue microenvironment. Many existing differentiation protocols mimic human brain macrophage developmental trajectories, but these protocols rely either on multi-step cytokine cocktails and lengthy differentiation or transduction of multiple transcription factors, both of which introduce variability and complicate genetic manipulation. To address these limitations, we developed a simplified protocol that generates high-purity (>90% CD45+CD11b+) human iPSC-derived macrophage-like cells (iMacs) from cryopreservable erythro-myeloid progenitor (EMP)-like intermediates in 19 days, including a final 7-day maturation step driven by macrophage colony-stimulating factor (M-CSF) alone. Transcriptomic profiling reveals that iMacs show enrichment for phagocytic and lysosomal programs, processes integral to efferocytosis. At both the transcriptional and protein level, iMacs have higher expression of scavenger receptors such as CD36, CD163 and MRC1, and of AD risk genes such as TREM2. Functionally, iMacs show enhanced phagocytic uptake of diverse substrates relative to iPSC-derived microglia, including carboxylated latex beads, zymosan, amyloid-{beta} 1-42, and amyloid-{beta} 1-40, and exhibit expanded lysosomal mass. Robust TREM2 expression and signaling make iMacs a sensitive platform for interrogating TREM2 biology, with markedly higher phosphorylation of SYK and PLC{gamma}2 in response to TREM2 engagement compared to iPSC-derived microglia. iMacs also tolerate lipid-mediated siRNA transfection with high survival and knockdown efficiency, enabling rapid genetic perturbation of AD risk genes. Together, these features make iMacs a practical, scalable, and genetically tractable human macrophage model for studying the regulation and cell biology of core macrophage functions that are known to play critical roles in AD, aging, and other disorders.

neuroscience↗

bioRxiv2026

Inflections in adolescent cortical maturation signal psychopathology risk

Cerebral cortical maturation supports emotional, social, and cognitive development during adolescence1. Neurodevelopmental theories of psychiatric illnesses, which peak in onset around age 182, implicate subtle alterations in adolescent cortical development3. However, mechanistic links between cortical maturation and emergent psychopathology have remained elusive. This gap likely reflects a need for more nuanced understanding of cortical development4, larger, longitudinal samples powered to detect small effects,5 and more uniform image quality control.6 Using 29,482 structural MRI scans from 11,720 adolescents in the Adolescent Brain Cognitive Development (ABCD) study, we demonstrate reproducible differences in the contour and tempo of maturation across the cortical surface. Regional trajectories are robust to image quality variance and align with increasing functional specialization over time. Thicker cortex in early-maturing sensory regions predicts psychiatric symptoms as early as four years prior to their emergence, a pattern that subsequently spreads to association cortex. Overlap with spatially and temporally organized gene co-expression networks implicates prenatal programming of this sequence of maturation and its links to psychopathology. These findings present a novel, versatile neurodevelopmental framework for cortical maturation during adolescence that sequentially implicates sensory and association cortex in risk for emergent psychiatric symptoms.

neuroscience↗

bioRxiv2026

Linkage disequilibrium moderates how evolving genetic background shapes variant-level architecture

Evolutionary theory offers a unifying explanation for the genetics of complex traits and diseases by modeling how a trait and its genetic basis are maintained by evolutionary forces. A growing body of evidence suggests that linkage disequilibrium (LD) couples a variant's evolution to that of the genetic background it resides on. However, widely used single-variant theories omit this coupling between variants and the background, or hold the background fixed. We close this gap by developing a model of linkage LD evolution accounting for stabilizing selection, recombination, and genetic drift. The model deduces the genetic architecture of individual variants subject to the co-evolving genetic background. More efficient selection in larger populations is partially offset by slower decay of existing LD and increased generation of new LD. Conversely, noisier LD in smaller populations exposes the variants to episodes of stronger selection. We ask whether ancestry differences in the relationship between effect-size magnitude and minor allele frequency require different selection strengths or can arise from differences in demographic history alone. Stabilizing selection needs to be more than three times stronger in Africans than in Europeans under the constant-size demography, whereas an Out-of-Africa demography alone can explain most of the observed frequency-dependence gap. As this example indicates, selection strength is in general not identifiable from the frequency--effect-size relationship alone, because different combinations of selection and demographic history can produce the same pattern in data with further redundancy added by LD.

genetics↗

bioRxiv2026

Surfactant-Assisted Colorimetric Signal Enhancement in Paper-Based Glucose Sensing

Paper-based colorimetric sensors offer a low-cost and accessible platform for point-of-care (POC) analysis, but enzyme activity loss during coating and drying can weaken analytical signals and require high enzyme loadings or complex immobilization procedures. Although surfactants are widely used to improve wettability in paper-based assays, their potential contribution to colorimetric performance beyond these effects remains unclear. Here, we investigated surfactant-assisted colorimetric signal enhancement in a glucose assay implemented on a 96-puddle paper plate (96-PPP) and identified Tween 20 as the most effective surfactant. Its effect on detection performance became more pronounced as glucose oxidase (GOx) loading decreased; at 0.1 mg/mL GOx, Tween 20 lowered the limit of detection (LoD) from 0.113 to 0.034 mg/mL (approximately 3.3-fold) over a working range of 0-5 mg/mL, despite no statistically significant change in the measured contact angle at this loading. Tween 20 had no appreciable effect on the reaction in solution but preserved 95% of the apparent reaction rate constant after drying, compared with 11% without it, and atomic force microscopy (AFM) revealed a more dispersed dried enzyme morphology on mica. Tween 20-containing sensors also showed slower signal decay during repeated wetting-drying cycles and thermal stress, retained 77% (vs 26%) of the response at 400 mM NaCl, and exhibited within-PPP and between-batch coefficients of variation (CVs) below 10% (vs 12.3-19.5%), while maintaining glucose selectivity over potentially interfering molecules. These results indicate that Tween 20 enhances paper-based glucose sensing beyond wettability, in part by retaining enzyme cascade activity during drying, although the contributions of the individual enzymes and the underlying mechanism remain to be established.

bioengineering↗

bioRxiv2026

DNMT1-Mediated Epigenetic Reprogramming Drives KMT2A Amplifications and Rearrangements

MLL/KMT2A amplifications and rearrangements are prevalent in infant, adult, and therapy-induced leukemia; however, the molecular contributors controlling these alterations remain elusive. Here, we reveal that rapid CTCF degradation generates local genome structure alterations at KMT2A and copy gains and rearrangements. We then established a conserved, coordinated interplay between DNA and histone methylation pathways that control CTCF occupancy, and in turn, KMT2A locus stability. For example, DNMT1 overexpression promotes increased H3K9 methylation, reduced CTCF occupancy, and causes KMT2A alterations. However, DNMT1 inhibition suppresses these events and KMT2A alterations caused by topoisomerase II inhibition. Locus-specific epigenome targeting demonstrated that DNA or H3K9 methylation promotes KMT2A copy gains and rearrangement, whereas targeted TET activity suppresses these events upon methylation perturbation or doxorubicin treatment. These findings identify a conserved, coordinated DNA-histone methylation axis governing KMT2A amplifications and rearrangement susceptibility, revealing biomarkers and therapeutic targets to predict and intercept these events in cancer.

cancer biology↗

bioRxiv2026

Cascaded Nano-ring Dialyzer for Continuous Regenerative Peritoneal Dialysis

End-stage kidney disease (ESKD) requires lifelong kidney replacement therapy, yet conventional hemodialysis and peritoneal dialysis remain limited by intermittent treatment, restricted mobility, and repeated dialysate exchange. Here, we developed a continuous regenerative peritoneal dialysis platform based on a nano-ring-assisted nanoelectrokinetic dialyzer for portable artificial kidney applications. We first identified key geometric and electrokinetic parameters governing the removal performance of nano-ring meshes, including mesh dimension, nano-ring coating thickness, the number of cascaded nano-rings, and the relative orientation between fluid flow and the applied electric field. We then developed a single nano-ring dialyzer operating at 1.33 mL/min and scaled the treatment capacity to approximately 10 mL min/min through parallel integration of multiple modules. In a canine model, the closed-loop system achieved approximately 10 % reduction in circulating uremic toxin levels during continuous treatment. We further improved the biocompatibility of the regenerated dialysate by integrating plate-type electrodes, activated carbon, bicarbonate buffering, and UV-C treatment. In an unanesthetized canine model, the improved system sustained continuous toxin removal for 4 h while major hepatic and inflammatory markers remained within recoverable ranges. These results demonstrate that cascaded nano-ring enables continuous dialysate regeneration with scalable throughput, reduced dependence on fresh dialysate, and in vivo control of uremic toxins, providing a technological foundation for portable or wearable regenerative peritoneal dialysis systems.

bioengineering↗

bioRxiv2026

Hygrochastic Seedpods: Engineering Microclimates for Forest Restoration

Forest restoration at scale depends on sowing seeds directly onto the land, yet seedling establishment is often poor and inconsistent. Seed enhancement technologies, such as priming, coating, and pelleting, improve germination under water, temperature, and salinity stress by supplying polymers, nutrients, or microorganisms at the seed surface. Being mainly conformal films, they act continuously once wetted and cannot gate when a seed is exposed to the soil. They also enclose no air volume, so the microenvironment they create is inseparable from the surrounding soil and has been inferred from plant performance rather than measured directly. Whether an engineered carrier can instead set both the state and the duration of the post-dispersal microenvironment, and how such an effect can be directly quantified, remains unexplored. Here we show that hygrochastic seedpods hold seeds in a timed, directly measurable microclimate and accelerate seedling emergence. The pods are programmable, responsive conical shells enclosing an air cavity around the seed. Two design solutions were investigated in parallel: wooden seedpods that crack open upon hydration, and poly(vinyl alcohol)/boric acid seedpods that gradually disintegrate after sustained wetting. In both, wax coatings act as a programmable diffusion-limited timer that sets activation from hours to days. The pod cavity permits direct sensing and monitoring, which no coating geometries allow. As directly measured during the initial phase after deployment, seedpod interiors ran 2 - 3 C warmer and drier than the surrounding soil, and these differences persisted after opening. Across indoor and field trials in several tree species, pods accelerated early seedling emergence without penalizing subsequent growth. These results identify artificial hygrochastic seedpods as a transient ecological mediator that regulates both the timing of seed exposure and the microclimate around the seed, offering a strategy for improving forest restoration under variable environmental conditions.

bioengineering↗

bioRxiv2026

Beyond codon optimality: codon pairs regulate mRNA stability dependent on translation

The coding sequence of an mRNA directs its own decay, yet how codons, codon context, and amino acids collectively regulate mRNA stability remains poorly understood. Here we use a massively parallel reporter assay to decode this regulatory layer in zebrafish embryos. We find that codon pairs and amino acid pairs regulate mRNA stability beyond the level of individual codons. This regulation depends on the identity and order of neighboring codons and their encoded amino acids in a translation-dependent manner. The relative contributions of codon and amino acid combinations to mRNA stability can be quantified using machine learning. We further found that endogenous mRNAs are regulated by codon pairs, thereby governing developmental gene regulation and biological function. This codon context-dependent decay requires deadenylation and decapping by Cnot7 and Dcp2, with Upf1 acting on long non-optimal ORFs. Together, our results redefine codon optimality as a context-dependent, pair-level code with implications for RNA biology and therapeutic mRNA design.

molecular biology↗

bioRxiv2026

Blockade of Kv3.1 by MK-801, a PCP-Derivative NMDA Receptor Inhibitor: Implications for Models of Schizophrenia

MK-801, a phencyclidine (PCP) derivative also known as dizocilpine, is a potent noncompetitive antagonist of the N-Methyl-D-aspartate receptor (NMDAr). The NMDAr plays a critical role in mediating excitatory synaptic transmission in the central nervous system (CNS) and is important in regulating synaptic plasticity, learning, and memory. MK-801 is known to induce schizophrenia-like phenotypes in animal models by blocking the NMDAr. Several studies have reported that the cognitive impairment associated with schizophrenia is linked to functional defects of ion channels in parvalbumin-positive GABAergic interneurons. Kv3.1 is a voltage-gated K+ (Kv) channel involved in the rapid repolarization of the action potential in neurons; it is richly expressed in parvalbumin-positive GABAergic interneurons and is associated with fast, repetitive spike generation. A decrease of Kv3.1 in the CNS has been reported to be associated with schizophrenia. In the present study, the effect of MK-801 on Kv3.1 was investigated using the whole-cell patch-clamp technique in Chinese hamster ovary (CHO) cells stably expressing Kv3.1. MK-801 caused a concentration-dependent inhibition of Kv3.1, with an IC50 of 10.81 M and a Hill coefficient of 0.89. The blocking potency was stronger at depolarized potentials, indicating a voltage-dependent block. MK-801 also produced a use-dependent block, inducing progressive inhibition with repeated stimulation at increased frequencies (1 Hz and 2 Hz), consistent with a delay in recovery from inactivation of Kv3.1 in the presence of MK-801. In addition, MK-801 induced a hyperpolarizing shift in the voltage dependence of the steady-state inactivation curve of Kv3.1. Taken together, these results indicate that MK-801 blocks Kv3.1 expressed in CHO cells in a concentration-, voltage-, and state-dependent manner. Given the importance of Kv3.1 in parvalbumin-positive, fast-spiking GABAergic interneurons, these findings suggest that MK-801 may alter the firing patterns of these inhibitory neurons, contributing to the onset and symptoms of schizophrenia.

pharmacology and toxicology↗

bioRxiv2026

Cortical and Hippocampal Pathways to Mental Continuity

How do people preserve mental continuity when tasks are interrupted? One established pathway runs through the hippocampus, which stores snapshots of our mental context for later reinstatement. We propose a second pathway: the brain's default network sustains the interrupted situation as a background process while other processing continues. In 73 adults listening to interrupted stories during functional brain imaging, the posterior medial cortex sustained a reliable and selective representation of the stages of the interrupted narrative. This background representation changed gradually over narrative time and persisted in a transformed format through silence and through a demanding secondary task. Its persistence predicted how reliably the default network resumed the story and how well listeners later recalled it, revealing complementary hippocampal and cortical pathways to mental continuity.

neuroscience↗

bioRxiv2026

Neural signatures of spontaneous transitions between internal and external thought

The human mind constantly shifts between internal representations and the external environment, yet the neural mechanisms underlying such spontaneous transitions remain underexplored. Here, we analyzed a think-aloud functional magnetic resonance imaging dataset, in which participants continuously verbalized their thoughts, to identify neural activity predicting transitions between internally and externally oriented thought. Internal-to-external transitions were preceded by increased activation in the salience/ventral attention network, with the strongest effect observed in the right temporoparietal junction. The spatial pattern of this pre-transition activation was positively associated with acetylcholine receptor density, suggesting a role for cholinergic signaling in cognitive reorientation. Pre-transition activation was itself preceded by a large-scale brain state proposed to serve as a flexible hub between functionally specialized states, indicating that spontaneous transitions are more likely when the brain occupies this intermediate configuration. Together, these findings suggest that multilevel neural mechanisms support flexible reorientation along the internal-external dimension of spontaneous cognition.

neuroscience↗

bioRxiv2026

Ancient Somatosensory Circuit Architectures Employ Flexible Molecular Strategies

The extent to which conserved neural circuit architectures depend on shared molecular specification programs remains unclear. Here, we address this question by examining the somatosensory system of the little skate, Leucoraja erinacea, an early-diverging vertebrate that retains ancestral features of both finned and limb-based body plans. We show that core features of somatosensory circuit organization, including laminar organization of the spinal cord and dorsally restricted targeting of sensory afferents, are deeply conserved. Unexpectedly, the molecular programs specifying dorsal root ganglion (DRG) sensory subtypes diverge extensively from those of mammals. Although DRG neuron subtype specification and spinal connectivity rely on target-derived cues, skates employ distinct neurotrophin receptor and transcription factor identity codes. These findings support a model in which conserved spinal circuit architectures provide a stable scaffold that leverages flexible sensory neuron specification programs, enabling the evolutionary diversification of vertebrate somatosensory systems.

neuroscience↗

bioRxiv2026

Immunizing small cell lung cancer mice with isoaspartylated Elavl4 after chemotherapy mimics improved survival of anti-ELAVL4 antibody-positive small cell lung cancer patients

Introduction: Small cell lung cancer (SCLC) patients have an ~8% 5-year survival; new therapies are urgently needed. Approximately 15% of SCLC patients have naturally-occurring low-titer antibodies against neuronal ELAVL proteins, associated with improved response to therapy and significantly improved survival. We previously determined that the anti-ELAVL4 response is triggered by isoaspartylation in the unstructured ELAVL4 N-terminal region. Methods: We used a Tp53fl/fl;Rb1fl/fl inducible SCLC mouse model to test whether 1) immunization with isoaspartylated Elavl4 (isoAsp-Elavl4) prior to SCLC induction improves survival in the absence of any other treatment, and 2) immunization with isoAsp-Elavl4 following completion of 3 rounds of cisplatin+etoposide therapy improves survival. Immunizations contained incomplete Freund's adjuvant with either a recombinant N-terminal fragment of Elavl4 (amino acids 1-117), incubated under isoaspartyl-inducing conditions, or phosphate-buffered saline (used as the negative control, since Elavl4 spontaneously isoaspartylates). Mice were monitored by blinded assessors until euthanasia was indicated. Results: IsoAsp-Elavl4-immunized animals all became immune responsive, and spontaneous anti-isoAsp-Elavl4 antibodies were observed in 7% of the control animals. Kaplan-Meier analyses revealed that pre-SCLC immunization with isoAsp-ELAVL4 in the absence of other treatments did not affect survival. In contrast, immunization of SCLC mice following chemotherapy significantly improved survival. Conclusions: An anti-isoAsp-ELAVL4 response can be actively induced in mice and significantly increases SCLC survival when given following chemotherapy. This indicates that the anti-isoAsp-ELAVL4 immune response can be leveraged to develop new therapies for SCLC patients.

cancer biology↗