Biology subjects

Dang, Y.

Publications and source records attributed to Dang, Y..

At least 19 recordsLinked to original sources

bioRxiv2026

A patient-centric therapeutic paradigm uncouples prostate cancer suppression from systemic metabolic collapse

The clinical benefits of cancer therapies are often compromised by the tolerable adverse effects that impair systemic organismal health and may evolve into latent life threats. Here, we identified profound abiraterone-induced but androgen-independent metabolic perturbations in prostate cancer patients and developed Lifehug-9892 to balance tumor therapy with systemic metabolic homeostasis. By integrating population cohorts with high-resolution metabolomics, we demonstrate that abiraterone induces profound systemic lipidomic dysregulation, characterized by the massive, pathological accumulation of desmosterol. Abiraterone inhibits but stabilizes DHCR24, leading to a metabolic trap in patients showing elevated levels of both desmosterol and cholesterol. Desmosterol accumulation is highly lipotoxic, potently triggering endothelial cell senescence and necrosis, macrophage foam cell formation, murine atherosclerosis, and hepatic senescence. To mechanistically uncouple and therapeutically rescue this systemic metabolic collapse, Lifehug-9892 was rationally designed to selectively retain on-target CYP17A1 inhibition while completely sparing DHCR24 function. Lifehug-9892 maintains potent tumor-suppressive activity while fully preserving the desmosterol-cholesterol metabolic axis and preventing systemic cardiovascular and hepatic damage. Our study uncovers a critical mechanistic link between drug-induced metabolic dysregulation and organismal health in cancer patients, providing a biochemical framework for developing patient-centric targeted therapies that preserve host homeostasis.

cancer biology↗

bioRxiv2026

Neuromodulation of Foxp2+ hypothalamic neurons induces therapeutic hypothermia

The inability to selectively trigger therapeutic hypothermia independent of environmental cooling has hindered causal analysis of its broader physiological benefits. Here, we employed P57, a natural product that pharmacologically induces therapeutic hypothermia circumventing external cold stress, to identify the neuronal substrates underlying hypothermia-induced antitumor effects. Integrating functional ultrasound imaging, activity-dependent neuronal labeling, and single-nucleus RNA sequencing, we identify a previously unrecognized population of Foxp2 neurons in the medial preoptic area (MPA) that are selectively activated by P57. Inhibition of MPA Foxp2+ neurons abolishes P57-induced hypothermia, whereas the paraventricular hypothalamus (PVH) serves as a critical downstream node. Importantly, targeted activation of MPA Foxp2 neurons is sufficient to induce sustained hypothermia, suppress systemic metabolism, and inhibit tumor growth, providing causal evidence that neuronally driven reductions in core body temperature can exert antitumor effects. Together, these findings establish MPA Foxp2 neurons as a controllable node for therapeutic hypothermia induction and demonstrate that neuromodulation of defined neuronal populations can achieve therapeutic benefit by directly controlling physiological states.

neuroscience↗

bioRxiv2026

Co-evolution of Oncogenic KRAS Signaling and LILRBhigh Macrophages Drives Pancreatic Cancer Recurrence

Pancreatic ductal adenocarcinoma (PDAC) frequently recurs after surgical resection, indicating that residual disease is sustained by coordinated tumor-microenvironment interactions. To define the biological basis of recurrence, we leverage large-scale clinical data from 2,710 patients, deeply characterized multi-omics profiling (whole-exome, bulk RNA, and single-nucleus sequencing) of 36 matched primary and locally recurrent PDACs, an in-house multiplex spatial imaging cohort of 190 patients, and extensive public datasets. Recurrent tumors were characterized by increased KRAS mutant allele dosage and reinforced KRAS signaling, accompanied by expansion of basal-like malignant cell states. In parallel, we identified an immunosuppressive macrophage population marked by high LILRB expression that spatially co-localized with KRAS-activated tumor cells. Functional studies showed that LILRB4+ macrophages enhanced tumor cell plasticity and progression, whereas inhibition of macrophage LILRB4 suppressed these phenotypes. Notably, a first-in-class human anti-LILRB4 antibody reduced macrophage-driven tumor traits, and dual targeting of KRAS signaling and LILRB4 achieved superior tumor control in macrophage-containing mouse models. These findings reveal a co-evolved tumor-immune niche underlying PDAC recurrence and nominate the KRAS-LILRB4 axis as a therapeutic vulnerability.

cancer biology↗

bioRxiv2026

Dysregulation of "Don't Eat Me" Signaling-Related Genes in Sepsis: A Targeted Transcriptomic Analysis

Sepsis remains a life-threatening condition with limited therapeutic options targeting immune dysregulation. The CD47-SIRP "dont eat me" signaling axis, well characterized in tumor immune evasion, has not been systematically investigated in the context of sepsis. In this study, we performed a targeted transcriptomic analysis of phagocytosis- and "dont eat me" -related genes using the GSE228541 dataset (14 sepsis patients, 15 healthy controls). We identified 8 significantly differentially expressed genes within the curated gene panel. Key changes included downregulation of CD47 (logFC = -0.88, FDR = 5.6 x 10-4) and marked upregulation of PRTN3 (logFC = 2.68, FDR = 6.1 x 10-4). Gene Ontology (GO) enrichment demonstrated prominent alterations in pathways including negative regulation of phagocytosis (GO:0050765, FDR = 7.6 x 10-22), endocytosis, and inflammatory responses. Co-expression network analysis identified SNX3, DYSF, and PLSCR1 as hub genes within this regulatory module. Immune infiltration analysis showed increased M1 macrophage polarization and neutrophil activation in sepsis. Using LASSO regression, we constructed a 6-gene diagnostic signature (PLSCR1, SNX3, DYSF, PRTN3, CSK, CD47) that discriminated sepsis from controls with good performance (AUC = 0.933 in the test subset). Downregulation of CD47 suggests impaired "self" recognition, which may contribute to aberrant phagocytosis during sepsis. Elevated PRTN3 is consistent with neutrophil activation and extracellular trap formation, linking innate immune activation to tissue injury. This targeted transcriptomic analysis reveals coordinated transcriptional reprogramming of phagocytosis-regulatory genes in sepsis and supports the CD47-SIRP axis as a candidate therapeutic target for further investigation.

bioinformatics↗

bioRxiv2026

p300/CBP-Driven Acetylation Stabilizes PARP7 to Reinforce Negative Feedback on IFN-I Signaling

Immune suppression within the tumor microenvironment (TME) remains a major barrier to effective immunotherapy, yet the molecular mechanisms that constrain type I interferon (IFN-I) signaling in tumor cells are incompletely understood. PARP7 (also known as TIPARP), a mono-ADP-ribosyltransferase, has been reported to suppress IFN-I signaling by modifying TBK1. Here, we identify PARP7 as a previously unrecognized acetylation substrate of the histone acetyltransferases p300 and CBP. We show that p300/CBP-mediated acetylation of PARP7 at lysine 32 markedly enhances its stability, thereby reinforcing repression of the TBK1-IRF3-STAT1 axis and suppressing IFN-{beta}-induced expression of interferon-stimulated genes, including CXCL10. Beyond their established function as transcriptional co-activators that support tumor cell proliferation, our findings uncover a direct role for p300/CBP in shaping innate antitumor immunity. Pharmacological inhibition of p300/CBP catalytic activity by A-485 abolishes PARP7 acetylation, accelerates its proteasomal turnover, and restores IFN-I signaling. In immunocompetent tumor models, this is accompanied by enhanced CD8+ T-cell infiltration and effector function. Together, these findings define a p300/CBP-PARP7 regulatory axis, uncover a non-canonical role for p300/CBP in innate immune suppression, and nominate this pathway as a tractable target for restoring antitumor immunity.

cancer biology↗

bioRxiv2026

Identification of an epigenetically and phenotypically distinct peritumoral glioblastoma cell population linked to inferior patient outcome

Glioblastoma (GB) is an aggressive and therapy-resistant primary brain tumor with dismal prognosis. Lethality is in most patients caused by a local peritumoral (Edge) relapse near the resection cavity. This region is insufficiently studied and experimental models are scarce. We have analyzed matched tissue samples and cell cultures from bulk tumors and Edge regions of 11 GB patients. Genomic profiling displayed similar genetic alterations and subclonal distributions of matched bulk and Edge regions. Functional, phenotypic and combined single nucleus (sn) RNA-seq and ATAC-seq analyses showed distinct differences between bulk and Edge GB cells with similar shifts across patients. Sn multiomics uncovered a subset of Edge cells defined by unique chromatin accessibility signatures and elevated mesenchymal and immune gene expression. Integrated computational and functional investigations converged on microglia-derived Oncostatin-M as a driver of the Edge-unique phenotype, and high expression of Edge-related signatures correlated with inferior patient outcome in independent GB cohorts.

cancer biology↗

bioRxiv2026

Hidden stop codons orchestrate mRNA fate by ambushing ribosomal frameshifting associated with codon usage

In eukaryotes, the mRNA stability is generally shaped by codon usage bias, the uneven preferences for synonymous codons, in a translation-dependent manner. However, the conserved mechanism linking codon to mRNA decay remains elusive. Hidden stop codons (HSCs), defined as stop codons located in the +1 or -1 frame relative to canonical ORF, are widespread across all genomes but largely uncharacterized. Here, we demonstrate that in both fungi and human cells, HSCs play an conserved and mechanistic role in promoting mRNA decay by rapidly terminating out-of-frame translation promoted by nonoptimal codons, primarily through +1 ribosomal frameshifting. In the filamentous fungus Neurospora crassa, partially deleting HSCs via synonymous substitutions in the clock gene frequency increases mRNA stability and disrupts circadian rhythmicity. In human cells, acute depletion of translation termination factor eRF1 impairs recognition of HSCs, leading to global stabilization of mRNAs enriched in nonoptimal codons and HSCs. In both Neurospora and humans, these mRNAs are in part degraded through the NMD pathway via UPF1. Collectively, these findings suggest that in eukaryotes, HSCs serve as surveillance elements to monitor ribosomal frameshifting and out-of-translation promoted by nonoptimal codons, thereby initiating mRNA decay through NMD.

molecular biology↗

bioRxiv2025

Dynamic interactions in human amygdala subregions support hierarchical processing of fearful faces

Fearful-expression recognition is critical for adaptive responses to potential threats and relies on both rapid threat detection and fine-grained face encoding. Yet how human amygdala subregions differentially support these distinct cognitive components remains unclear. Here, we recorded intracranial EEG from lateral and medial amygdala in epilepsy patients performing an emotional face-matching task and combined multivariate decoding, time-frequency and directed-connectivity analyses with intracranial stimulation. The lateral amygdala exhibited early fear-specific responses, characterized by higher decoding accuracy and increased theta/alpha-band (4-12 Hz) power, and transmitted this fear-related information to the medial amygdala, which showed delayed and sustained activation. By contrast, the medial amygdala encoded face-specific information at later stages in the 2-16 Hz band with superior decoding accuracy and then relayed this information back to the lateral amygdala. Intracranial stimulation produced a double dissociation in behavior, with lateral amygdala stimulation disrupting fear detection, whereas medial amygdala stimulation selectively accelerated neutral-face recognition. Together, these findings reveal a temporal hierarchy in the human amygdala, whereby dynamic bidirectional interactions between subregions implement distinct components of fearful-expression recognition, providing a circuit-level framework for understanding social threat processing.

neuroscience↗

bioRxiv2025

Collective Gene Expression Fluctuations Encode the Regulatory State of Cells

Gene expression is inherently stochastic, leading to substantial cell-to-cell variability in mRNA and protein abundances. Variability in the expression of individual genes has been associated both with impaired signal processing and with facilitation of stress responses and differentiation. Here, combining machine learning, theory, and analysis of scRNA-seq data across various organisms and tissues, we show that variability in gene expression can be coordinated cell-wide. We define a statistical score that quantifies this coordination in single-cell data and demonstrate that distinct coordination patterns reflect the regulatory state of cells. We further develop a physics-informed machine-learning framework that identifies and predicts such variability patterns. Coordinated gene-expression variability emerges as a hallmark of stem and progenitor cells and distinguishes intrinsic stochasticity from cell-population heterogeneity. Together, our results establish the structure of gene expression variability as a cellular-scale signature of cell identity and regulatory organization.

biophysics↗

bioRxiv2024

Adaptation to cystine limitation stress promotes PDAC tumor growth and metastasis through translational upregulation of OxPPP

Cystine/cysteine is critical for antioxidant response and sulfur metabolism in cancer cells and is one of the most depleted amino acids in the microenvironment of pancreatic ductal adenocarcinoma (PDAC). The effects of cystine limitation stress (CLS) on PDAC progression are poorly understood. Here we report that adaptation to CLS (CLSA) promotes PDAC cell proliferation and tumor growth through translational upregulation of the oxidative pentose phosphate pathway (OxPPP). OxPPP activates the de novo synthesis of nucleotides and fatty acids to support tumor growth. On the other hand, CLSA-mediated lipidomic reprogramming depends on triacylglycerides synthesis and lipid droplet formation to mitigate lipotoxicity. Through drug screening, we identify lomitapide as an inhibitor of CLSA PDAC tumor growth and a potent sensitizer of chemotherapy. Lomitapide inhibits triacylglycerides synthesis to interfere with CLSA and chemotherapy-induced lipidomic reprogramming. Taken together, we demonstrate that CLSA promotes PDAC tumor growth through metabolic reprogramming and lomitapide could be used to target the dysregulated lipid metabolism in PDAC.

cancer biology↗

bioRxiv2024

p300/CBP-catalyzed acetylation safeguards minor zygotic genome activation via activating DUX

Zygotic genome activation (ZGA), the first transcriptional event at the onset of life, is crucial for early embryonic development. However, the mechanisms that initiate and regulate ZGA in mammals remain poorly understood. In this study, we demonstrate that p300/CBP-catalyzed acetylation plays a vital role in regulating ZGA. Inhibition of p300/CBP acetyltransferase activity results in impaired minor ZGA and a subsequent 2-cell arrest. By profiling the dynamic landscape of p300 during the ZGA stage, we elucidate the distinct patterns of p300 establishment in promoter and enhancer regions. Moreover, p300 recruits RNA polymerase (Pol II) to pre-configure in the promoter regions of ZGA genes, and orchestrates the gradual establishment of enhancer activity during the early 2-cell stage to activate ZGA. Furthermore, p300 enhances minor ZGA by promoting the expression of DUX. Restoring DUX levels, which are diminished due to p300/CBP inhibition, rescues ZGA and embryonic development by re-establishing Pol II enrichment on minor ZGA genes. Overall, our findings elucidate the mechanism by which p300/CBP regulates ZGA through acetylation and activation of the key transcription factor DUX. HighlightsO_LIp300/CBP plays a stage-specific role during preimplantation development phase. C_LIO_LIp300 displays distinctive dynamic changes in promoter and enhancer regions during ZGA stage. C_LIO_LIp300/CBP-catalyzed acetylation facilitates the pre-configuration and elongation of Pol II at ZGA gene regions. C_LIO_LIDUX recruits p300 and Pol II to activate minor ZGA genes independently of p300s catalytic activity. C_LI

developmental biology↗

bioRxiv2024

A unified central thalamus mechanism underlying diverse recoveries in disorders of consciousness

Disorders of consciousness (DoC) encompass a range of states characterized by prolonged altered awareness due to heterogeneous brain damage and are associated with highly diverse prognoses. However, the neural mechanisms underlying such diverse recoveries in DoC remain unclear. To address this issue, we analysed neuronal spiking activities recorded from the central thalamus (CT), a key hub in arousal regulation, in a cohort of 23 DoC patients receiving deep brain stimulation treatment. Using machine learning techniques, we identified a core set of electrophysiological features of the CT, particularly the theta rhythm, that could account for individual recovery outcomes across highly varied etiologies (trauma, brainstem hemorrhage, and anoxia), clinical baselines and patient ages. These features also correctly identified one subgroup of patients who exhibited poor initial clinical manifestations but recovered unexpectedly. Simulating a conductance-based model further revealed the neurodynamics of the theta rhythm in the CT during different stages of consciousness recovery. Taken together, these findings uncover a previously unknown, unified CT mechanism that governs the recoveries in DoC.

neuroscience↗

bioRxiv2024

Spatial dynamics of mammalian brain development and neuroinflammation by multimodal tri-omics mapping

The ability to spatially map multiple layers of the omics information over different time points allows for exploring the mechanisms driving brain development, differentiation, arealization, and alterations in disease. Herein we developed and applied spatial tri-omic sequencing technologies, DBiT ARP-seq (spatial ATAC-RNA-Protein-seq) and DBiT CTRP-seq (spatial CUT&Tag- RNA-Protein-seq) together with multiplexed immunofluorescence imaging (CODEX) to map spatial dynamic remodeling in brain development and neuroinflammation. A spatiotemporal tri-omic atlas of the mouse brain was obtained at different stages from postnatal day P0 to P21, and compared to the regions of interest in the human developing brains. Specifically, in the cortical area, we discovered temporal persistence and spatial spreading of chromatin accessibility for the layer-defining transcription factors. In corpus callosum, we observed dynamic chromatin priming of myelin genes across the subregions. Together, it suggests a role for layer specific projection neurons to coordinate axonogenesis and myelination. We further mapped the brain of a lysolecithin (LPC) neuroinflammation mouse model and observed common molecular programs in development and neuroinflammation. Microglia, exhibiting both conserved and distinct programs for inflammation and resolution, are transiently activated not only at the core of the LPC lesion, but also at distal locations presumably through neuronal circuitry. Thus, this work unveiled common and differential mechanisms in brain development and neuroinflammation, resulting in a valuable data resource to investigate brain development, function and disease.

neuroscience↗

bioRxiv2024

Pre-cancerous Niche Remodelling Dictates Nascent Tumour Survival

Interactions between mutant cells and their environment play a key role in determining cancer susceptibility. However, our understanding of how the pre-cancer microenvironment contributes to early tumorigenesis remains limited. Here, we show that newly emerging tumours at their most incipient stages shape their microenvironment in a critical process that determines their survival. Analysis of nascent squamous tumours in the upper gastrointestinal tract of the mouse reveals that the stress response of early tumour cells instructs the underlying mesenchyme to form a supportive "pre-cancer niche", which dictates the long-term outcome of epithelial lesions. Stimulated fibroblasts beneath emerging tumours activate a wound healing response that triggers a dramatic remodelling of the underlying extracellular matrix, resulting in the formation of a fibronectin-rich stromal scaffold that promotes tumour growth. Functional heterotypic 3D culture assays and in vivo grafting experiments, combining carcinogen-free healthy epithelium and tumour-derived stroma, demonstrate that the pre-cancerous niche alone is sufficient to confer tumour properties to healthy epithelial cells. We propose a model where both mutations and the stromal response to genetic stress defines the likelihood of early tumours to survive and progress towards more advanced disease stages.

cancer biology↗

bioRxiv2024

Transcriptional landscapes underlying Notch-induced lineageconversion and plasticity of mammary basal cells

The mammary epithelium derives from multipotent mammary stem cells (MaSCs) that progressively restrict their potency and engage into lineage commitment during embryonic development. Although postnatal mammary progenitors are lineage-restricted and unipotent, several lines of evidence have documented their extensive plasticity and ability to reactivate multipotency in several non-physiological contexts. We have previously shown that ectopic Notch1 activation in committed mammary basal cells, which never experience Notch activity in homeostatic conditions, triggers a progressive cell fate switch from basal to luminal cell identity in both the pubertal and adult mouse mammary gland. Here, we tested the conservation of this mechanism in other glandular epithelia and found that constitutive Notch1 signaling also induces a basal-to-luminal cell fate switch in adult cells of the lacrimal gland, the salivary gland, and the prostate. Since cells do not undergo lineage transition synchronously and this switch is progressive in time, we performed single cell transcriptomic analysis by SMART-Seq on index-sorted mutant mammary cells at different stages of lineage conversion, to reveal the molecular pathways underlying the fate transition. Combining single cell transcriptomics analyses with assays in organoid cultures, we demonstrate that proliferation of basal mutant cells is indispensable to convert them into luminal progenitors. We thus reveal the molecular mechanisms and individual transcriptional landscapes controlling lineage conversion and cellular plasticity of unipotent committed mammary cells in vivo with spatial and temporal resolution. Given the strong implications of Notch signaling in cancer, these results also provide important insights into the mechanisms that drive cellular transformation.

developmental biology↗

bioRxiv2024

Intracranial neural representation of phenomenal and access consciousness in the human brain

After more than 30 years of extensive investigation, impressive progress has been made in identifying the neural correlates of consciousness (NCC). However, the functional role of spatiotemporally distinct consciousness-related neural activity in conscious perception is debated. Based on empirical EEG findings, e.g., of the enhanced early negative wave and late positive wave under conscious conditions, an influential framework proposed that consciousness-related neural activities could be dissociated into two distinct processes: phenomenal and access consciousness. This framework has been supported mainly by comparison of neural activity between report and no-report paradigms; however, though hotly debated, its authenticity has not been examined in a single paradigm with more informative intracranial recordings. In the present study, we employed a novel visual awareness task and recorded the local field potential (LFP) of epilepsy patients with electrodes implanted in cortical and subcortical regions. Overall, we found that the latency of visual awareness-related activity exhibited a bimodal distribution, and the recording sites with short and long latencies were largely separated in location, except in the lateral prefrontal cortex (lPFC). The mixture of short and long latencies in the lPFC indicates that it plays a critical role in linking phenomenal and access consciousness. However, the division between the two is not as simple as the central sulcus, as proposed previously. Moreover, in 4 patients with electrodes implanted in the bilateral prefrontal cortex, early awareness-related activity was confined to the contralateral side, while late awareness-related activity appeared on both sides. Finally, Granger causality analysis showed that awareness-related information flowed from the early sites to the late sites. These results provide the first LFP evidence of neural correlates of phenomenal and access consciousness, which sheds light on the spatiotemporal dynamics of NCC in the human brain.

neuroscience↗

bioRxiv2024

Human intralaminar and medial thalamic nuclei transiently gate conscious perception through the thalamocortical loop

Human high-order thalamic nuclei have been known to closely correlate with conscious states. However, given the great difference of conscious states and contents (conscious perception), it is nearly unknown how those thalamic nuclei and thalamocortical interactions directly contribute to the transient process of conscious perception. To address this question, we simultaneously recorded local field potentials (LFP) in the human intralaminar, medial and ventral thalamic nuclei as well as in the prefrontal cortex (PFC), while patients with implanted electrodes performing a visual consciousness task. Overall, compared to the ventral nuclei, intralaminar and medial nuclei showed earlier and stronger consciousness-related activity. Moreover, the transient thalamocortical neural synchrony and cross-frequency coupling were both driven by the theta phase of the intralaminar and medial nuclei during conscious perception. These results indicated that the intralaminar and medial thalamic nuclei, rather than the commonly believed PFC, play a decisive gate role in conscious perception. Highlights O_LIIntralaminar and medial thalamic nuclei showed earlier and stronger visual consciousness-related activity, comparing to the ventral nuclei. C_LIO_LIIntralaminar and medial thalamic transiently drove the thalamocortical synchronization through theta (2-8Hz) phase modulation during the emergence of visual consciousness. C_LIO_LITheta phase of intralaminar and medial thalamic activity dynamically regulated the amplitude of PFC activity during the emergence of consciousness. C_LIO_LIIntralaminar and medial thalamic nuclei showed more regulation on lateral PFC than on other PFC subregions during the emergence of consciousness. C_LI

neuroscience↗

bioRxiv2023

Epigenetic insights into GABAergic development in Dravet Syndrome iPSC and therapeutic implications

Dravet syndrome (DS) is a devastating early onset refractory epilepsy syndrome caused by variants in the SCN1A gene. A disturbed GABAergic interneuron function is implicated in the progression to DS but the underlying developmental and pathophysiological mechanisms remain elusive, in particularly at the chromatin level. In this study, we utilized induced pluripotent stem cells (iPSCs) derived from DS cases and healthy donors to model disease- associated epigenetic abnormalities of GABAergic development. Employing the ATAC-Seq technique, we assessed chromatin accessibility at multiple time points (Day 0, Day 19, Day 35, and Day 65) of GABAergic differentiation. Additionally, we elucidated the effects of the commonly used anti-seizure drug valproic acid (VPA) on chromatin accessibility in GABAergic cells. The distinct dynamics in chromatin profile of DS iPSC predicted accelerated early GABAergic development, evident at D19, and diverged further from the pattern in control iPSC with continued differentiation, indicating a disrupted GABAergic maturation. Exposure to VPA at D65 reshaped the chromatin landscape at a variable extent in different iPSC-lines and rescued the observed dysfunctional development in some DS iPSC-GABA. This study provides the first comprehensive investigation on the chromatin landscape of GABAergic differentiation in DS-patient iPSC, offering valuable insights into the epigenetic dysregulations associated with interneuronal dysfunction in DS. Moreover, our detailed analysis of the chromatin changes induced by VPA in iPSC-GABA holds the potential to improve development of personalized and targeted anti-epileptic therapies.

cell biology↗