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Biology subjects

Geng, Z.

Publications and source records attributed to Geng, Z..

At least 19 recordsLinked to original sources

InfluProto: Predicting Cross-Species Transmission of Influenza A Virus via Prototype Learning

Zoonotic influenza A viruses pose constitute a significant persistent threat to global public health, yet quantitative approaches for assessing their cross-species transmission potential remain limited. Here, we present InfluProto, a deep learning model that introduces prototype learning into host prediction for influenza A virus, framing conceptualizing host adaptation as a continuous process rather than a discrete outcome. InfluProto embeds viral sequences into a continuous representation space anchored by human, swine, and avian prototypes, using cosine distances as a quantitative measure of host adaptation. InfluProto accurately discriminated among the three host classes, achieving recall and precision exceeding 0.97, and substantially outperformed conventional classification models models--particularly on challenging zoonotic strains, including the 2009 pandemic H1N1 (pdm09) lineage. Beyond host classification, the learned representations captured biologically meaningful host-adaptive signatures,; notably, with pdm09 viruses occupying occupied an intermediate position between human and swine clusters, consistent with their evolutionary origin. Analysis of simulated reassortment further revealed that the introduction of human-origin segments into swine influenza viruses reduced their distance to the human prototype, indicating that InfluProto can detect reassortment-associated shifts in host adaptation. To facilitate broad public useaccess, we have developed an interactive web service for InfluProto. Collectively, our work establishes a continuous framework for characterizing host adaptation and evaluating zoonotic risk in influenza A viruses, with potential implications for pandemic surveillance and preparedness.

microbiology↗

LDB1-dependent enhancer connectivity defines T-cell leukemia identities and masks metabolic vulnerabilities

Spatial enhancer connectivity is fundamental to proper gene regulation. Enhancer dysregulation has emerged as a hallmark of cancers, including T-cell acute lymphoblastic leukemias (T-ALL). T-ALL are aggressive malignancies characterized by marked transcriptional heterogeneity driven by distinct stages of developmental arrest and diverse noncoding alterations. How these cancers co-opt nuclear architecture to rewire enhancer connectivity remains poorly understood. Here, we report that the LDB1 chromatin architectural complex is an essential mediator of enhancer-oncogene looping that sustains oncogenic transcriptional programs across multiple T-ALL subtypes. Integrating bulk and single-cell transcriptomic data from patients with T-ALL and healthy hematopoietic controls, we show that the LDB1-dependent regulatory circuitry defines the molecular identities of distinct T-ALL subtypes while restricting plasticity toward alternative cell states. LDB1 loss dismantles chromatin looping among cell state-defining enhancers liberating them to form promiscuous interactions with nearby genes. This enhancer rewiring stimulates expression of key metabolic genes, creating a mevalonate pathway dependency exploitable with statin treatment. Our study establishes LDB1 as a central executor of T-ALL regulatory circuitry and more broadly illustrates chromatin rewiring as a source of targetable dependencies in cancer.

Cancer Biology↗

Transcription factor CCTF1 plays a decisive role in regulating the proteasome activity during archaeal cell division

Archaea of the order Sulfolobales exhibit a highly ordered cell cycle progression similar to that of eukaryotes. It has been demonstrated that degradation of the cell division protein CdvB by the proteasome controls the progression of cell division. However, how the proteasome itself is regulated during the cell cycle is not fully understood. Recently, the cyclically expressed ArsR family transcription factor CCTF1 (cell cycle transcription factor 1) was shown to represses expression of PAN (proteasome-activating nucleotidase) in Sulfolobus acidocaldarius. Here, using biochemical approaches, comparative transcriptomics and proteomics, we provide further insights into the CCTF1 function and show that it regulates PAN expression in Saccharolobus islandicus by binding to an AT-rich palindromic sequence within the pan promoter. We also reassessed the role of the cyclically expressed protein kinase aCcrK in regulation of proteasome activity and conclude that CCTF1, rather than aCcrK, is the primary factor controlling the proteasome activity. These findings advance our understanding of the proteosome-mediated cell cycle regulation in archaea.

microbiology↗

Polymer-lipid hybrid nanoparticle enhances mRNA delivery and T cell-mediated immunity

mRNA vaccines have transformed prophylactic immunization against infectious diseases as well as therapeutic interventions for cancer. However, their effectiveness against emerging viral variants and a range of malignancies continues to be hindered by suboptimal induction of T cell-mediated immunity. To overcome this limitation, here we developed a polymer-lipid hybrid nanoparticle (PLNP) platform engineered to improve mRNA delivery to antigen-presenting cells (APCs) and to potentiate T cell responses. Relative to conventional mRNA lipid nanoparticle (LNP) vaccines, mRNA PLNP vaccines demonstrated markedly improved lymph node targeting, APC activation, Th1-biased pro-inflammatory cytokine response, and antigen-specific T cell expansion while retaining robust humoral immunity. Remarkably, mRNA-PLNP vaccines generated approximately 50% more antigen-specific CD8+ T cells than mRNA-LNP vaccines across multiple antigens, including SARS-CoV-2 spike, influenza hemagglutinin, and ovalbumin. In prophylactic applications, mRNA PLNP vaccine provided complete protection against SARS-CoV-2 variants. As a therapeutic approach in a melanoma model, mRNA PLNP vaccination resulted in enhanced tumor control and significantly prolonged survival compared to LNP-based formulations. Collectively, these results establish PLNP as a versatile and broadly applicable platform for augmenting mRNA vaccine efficacy through improved mRNA delivery and T cell priming, offering promising implications for infection prevention and cancer immunotherapy.

immunology↗

Complement Factor H (Y402H) polymorphism for age-related macular degeneration alters retinal lipids

Age-related macular degeneration (AMD), the leading cause of blindness in the elderly, is associated with multiple risk factors and involves death of the retinal pigment epithelium (RPE). We investigated how the Y402H polymorphism of Complement Factor H (CFH) and cigarette smoke extract (CSE), major AMD genetic and environmental risks, affect lipid metabolism in RPE differentiated from induced pluripotent stem cells (iPSC-RPE) that were derived from human donors genotyped for low-risk (LR) or high-risk (HR) CFH. Results from discovery-based (lipidomics, proteomics) and targeted (mitochondrial fatty acid oxidation (FAO)) assays found significant genotype-dependent differences under basal conditions include higher free fatty acids and cholesterol esters in HR cells. CSE induced differences in proteins regulating lipid handling, lipolysis, and inflammation. Lower FAO in HR cells was observed in multiple donors and pairs of parent/isogenic edited lines compared with LR lines. CSE induced lipid accumulation, lipid composition remodeling, and upregulation of proteins involved in lipid synthesis/hydrolysis, production of bioactive lipid mediators, and metabolism of ceramide and cholesterol. These results elucidate putative mechanisms driving pathology in RPE harboring CFH Y402H.

systems biology↗

A gene program dictionary of human cells

Defining all human cell types and their roles in health and disease is a central goal of biology. Single-cell RNA sequencing has enabled the construction of organ-specific cell atlases, but building a comprehensive organism-wide atlas spanning multiple organs remains challenging due to batch effects, study biases, and inter-organ complexity. Here, we present Gene Program Dictionary (GPD), a framework that leverages robust gene co-expression programs--rather than direct cell integration--to overcome these barriers. Using SpacGPA, a partial correlation-based network method, we analyzed 466 scRNA-seq datasets, generating 1,975 independent networks and 90,701 gene co-expression modules, which were consolidated into 1,534 consensus gene programs representing a wide range of human tissues and cell types. Each program serves as a composite marker, capturing both cell-type-specific and shared biological processes. We demonstrate their utility by mapping endothelial cell subtypes across tissues to reveal their heterogeneity--including tumor-specific programs--annotating colorectal cancer spatial transcriptomes, and linking programs and their corresponding cell types to disease loci, revealing hotspots such as neuronal programs in psychiatric disorders and a proximal tubule program in kidney diseases. GPD provides an organism-wide reference for studying cellular diversity and disease mechanisms.

bioinformatics↗

Three transcription factors coordinate the archaeal cell cycle progression through a regulatory braking point mechanism

Archaea of the order Sulfolobales execute a well-structured cell cycle program similar to that of eukaryotic cells. However, unlike eukaryotes, archaea lack cyclins and cyclin-dependent kinases and thus the mechanism of cell cycle regulation remained enigmatic. Here, we show that three essential ribbon-helix-helix domain transcription factors, namely, aCcr1, aCcr2, and aCcr3, play pivotal roles in controlling the cell cycle progression in the thermoacidophilic archaeon Saccharolobus islandicus. Coordinated expression of aCcr1 during M-G1 phase, aCcr3 during G1-S phase, and aCcr2 throughout the cell cycle ensures the timely transcription of the key genes that define the cell cycle phases. These include genes involved in chromosome dimer resolution, chromosome segregation, cell division, chromatin organization, DNA replication and repair, protein phosphorylation and degradation and metabolisms of amino acids, tRNA and carbohydrates. The synergy between aCcr1, aCcr2, and aCcr3 is achieved through their differencial affinities for the promoters and the levels of protein expression. We propose that the global regulation of the Sulfolobales cell cycle may be achieved not through transcriptional activation, but rather by repression of the key genes during strategic moments of the cell cycle. We propose a braking point model for the cell cycle control in Sulfolobales, which may represent a simple evolutionary intermediate on the way to the more complex cell cycle regulation in eukaryotes.

microbiology↗

Methionine γ-lyase Traps Cofactor Pyridoxal-5'-phosphate through Specific Serine-Mediated Affinity

Pyridoxal-5'-phosphate (PLP), the ubiquitous and ancient cofactor, plays important roles in enzymatic elimination, transamination and other reactions. The catalytic efficiency of PLP-dependent enzymes is significantly higher than that of free PLP. The recruitment of PLP from the environment by the enzymes, particularly through interactions outside the active site, is the key step determining the occurrence of PLP-mediated catalysis. However, the precise mechanism by which enzymes recruit PLP remains elusive. Methionine {gamma}-lyase (MGL), a PLP-dependent enzyme, catalyzes the degradation of L-methionine, thereby suppressing cancer cell proliferation through serum or dietary methionine depletion. Here, we report the crystal structure of yMGL, which belongs to a newly identified subgroup of cystathionine {gamma}-lyases, in complex with L-methionine and PLP. Through truncating the C-terminal domain of yMGL both in vitro and in vivo, we demonstrated that this domain, outside the canonical PLP-binding domain, is essential for the specific interaction between yMGL and PLP, as well as for efficient L-methionine catabolism. A conserved Ser in the C-terminal domain, positioned at the active-site entrance of MGLs, confers specificity for PLP. These findings elucidate a previously uncharacterized mechanism of PLP recruitment by MGLs and promote rational design of MGLs with tailored cofactor selectivity and catalytic performance.

biochemistry↗

CHIEF: An Attention-based Ensemble Learning Framework for Functional Protein Design

Protein de novo design is a longstanding challenge in biological field due to the multifaceted physicochemical properties and complexities of proteins. Several deep learning models have emerged for protein de novo design. However, each model exhibits distinct strengths and limitations because of the differences in training strategies or neural network architectures. Therefore, improving the effectiveness of protein design, particularly for functional protein, requires further improvement. To tackle this challenge, we developed CHIEF (Chimera Ensemble Inverse Folding), an attention-based ensemble framework that integrates five pretrained base models (ProteinMPNN-vanilla, ProteinMPNN-soluble, ESM-IF, Frame2seq and PiFold) to leverage their complementary strengths and mitigate limitations. Compared with the base models, CHIEF significantly improved the sequence recovery rate by 16.6-28.0%, while reducing the prediction perplexity by 22.7-34.6%. CHIEF also exhibited superior protein-designing capacity in variable sequence- and structure-based metrics and in large and complex proteins. CHIEF dynamically captured the semantic information from base models in a context-dependent manner and was minimally affected by the ablation of each base model. More importantly, CHIEF demonstrates real-world applicability to design functional malate dehydrogenase (MDH), achieving a 100% success rate. In summary, our study develops an ensemble deep learning model that improves the efficacy of protein sequence design, and will be a valuable platform for protein engineering and drug development.

bioengineering↗

The zinc-finger protein POGZ associates with Polycomb repressive complex 1 to regulate bone morphogenetic protein signaling during neuronal differentiation

Polycomb Repressive Complex 1 (PRC1) is a family of epigenetic regulators critical for mammalian development. Elucidating PRC1 composition and function across cell types and developmental stages is key to understanding the epigenetic regulation of cell fate determination. In this study, we discovered POGZ, a prominent Autism Spectrum Disorder (ASD) risk factor, as a novel component of PRC1.6, forming the PRC1.6-POGZ complex. Functional assays revealed that POGZ elicits transcriptional repression that is dependent on RING1B expression. Analysis of publicly available ChIP-Seq data showed that POGZ highly colocalizes with RING1B and HP1{gamma}, two PRC1.6 components, at genes involved in multiple aspects of transcriptional regulation in the embryonic mouse cortex. Although Pogz knockout (KO) does not compromise stem cell pluripotency, Pogz ablation in neuronal progenitor cells (NPCs) led to widespread transcriptomic dysregulation with failed activation of key neuronal genes. Finally, we demonstrated that PRC1.6-POGZ regulates neuronal differentiation by repressing the bone morphogenetic protein (BMP) signaling pathway. These findings reveal a mechanism by which PRC1 and POGZ coordinate transcriptional regulation during neuronal differentiation, which offers insights into how disruptions in this pathway may contribute to neurodevelopmental disorders such as ASD.

biochemistry↗

PRC1 and CTCF-Mediated Transition from Poised to Active Chromatin Loops Drives Bivalent Gene Activation

Polycomb Repressive Complex 1 (PRC1) and CCCTC-binding factor (CTCF) are critical regulators of 3D chromatin architecture that influence cellular transcriptional programs. Spatial chromatin structures comprise conserved compartments, topologically associating domains (TADs), and dynamic, cell-type-specific chromatin loops. Although the role of CTCF in chromatin organization is well-known, the involvement of PRC1 is less understood. In this study, we identified an unexpected, essential role for the canonical Pcgf2-containing PRC1 complex (cPRC1.2), a known transcriptional repressor, in activating bivalent genes during differentiation. Our Hi-C analysis revealed that cPRC1.2 forms chromatin loops at bivalent promoters, rendering them silent yet poised for activation. Using mouse embryonic stem cells (ESCs) with CRISPR/Cas9-mediated gene editing, we found that the loss of Pcgf2, though not affecting the global level of H2AK119ub1, disrupts these cPRC1.2 loops in ESCs and impairs the transcriptional induction of crucial target genes necessary for neuronal differentiation. Furthermore, we identified CTCF enrichment at cPRC1.2 loop anchors and at Polycomb group (PcG) bodies, nuclear foci with concentrated PRC1 and its tethered chromatin domains, suggesting that PRC1 and CTCF cooperatively shape chromatin loop structures. Through virtual 4C and other genomic analyses, we discovered that establishing neuronal progenitor cell (NPC) identity involves a switch from cPRC1.2-mediated chromatin loops to CTCF-mediated active loops, enabling the expression of critical lineage-specific factors. This study uncovers a novel mechanism by which pre-formed PRC1 and CTCF loops at lineage-specific genes maintain a poised state for subsequent gene activation, advancing our understanding of the role of chromatin architecture in controlling cell fate transitions.

genomics↗

The splicing modulator CLK1 is a candidate oncogenic dependency in pediatric high-grade gliomas

BackgroundPediatric brain tumors are the leading cause of disease-related mortality in children, yet many aggressive tumors lack effective therapies. RNA splicing is a hallmark of cancer, but it has not yet been systematically studied in pediatric brain tumors. MethodsWe analyzed 729 pediatric brain tumors spanning histologies and molecular subtypes to quantify differential tumor splicing. We developed the Splicing Burden Index (SBI) to enable cross-sample comparisons and performed hierarchical clustering of highly variable splice events to define splicing-informed tumor groups. These were integrated with clinical outcomes, pathway activity, and proteogenomic data. Recurrent splice events were prioritized for predicted functional impact, and in vitro perturbation studies were performed targeting the splicing kinase CDC-like kinase 1 (CLK1). ResultsSBI revealed substantial inter- and intra-histology heterogeneity. Clusters were enriched for histologies and molecular subtypes, several of which were independently associated with survival beyond histology and clinical covariates. Spliceosome pathway activity varied across clusters and was associated with worse survival, yet was not correlated with SBI, indicating distinct dimensions of splicing dysregulation. Functional prioritization identified a recurrent in CLK1 exon 4, required for canonical kinase activity. CLK1 exon 4 inclusion followed an oncofetal pattern and showed context-dependent associations with outcome distinct from total CLK1 expression. Pharmacologic inhibition and exon 4-specific perturbation of CLK1 reduced tumor cell viability and disrupted cancer-relevant splicing and transcriptional programs. ConclusionsThis study systematically characterizes splicing in pediatric brain tumors, identifies splicing-informed subgroups, and prioritizes CLK1 exon 4 as an oncofetal tumor-specific event, motivating further preclinical exploration. Key Points[bullet] Splicing analysis of 729 pediatric CNS tumors identifies splicing-defined clusters. [bullet]CLK1 exon 4 inclusion is widespread and developmentally regulated. [bullet]Exon-level CLK1 regulation shows context-dependent links to prognosis in aggressive CNS tumors.

genomics↗

The Open Pediatric Cancer Project

BackgroundIn 2019, the Open Pediatric Brain Tumor Atlas (OpenPBTA) was created as a global, collaborative open-science initiative to genomically characterize 1,074 pediatric brain tumors and 22 patient-derived cell lines. Here, we present an extension of the OpenPBTA called the Open Pediatric Cancer (OpenPedCan) Project, a harmonized open-source multi-omic dataset from 6,112 pediatric cancer patients with 7,096 tumor events across more than 100 histologies. Combined with RNA-Seq from the Genotype-Tissue Expression (GTEx) and The Cancer Genome Atlas (TCGA), OpenPedCan contains nearly 48,000 total biospecimens (24,002 tumor and 23,893 normal specimens). FindingsWe utilized Gabriella Miller Kids First (GMKF) workflows to harmonize WGS, WXS, RNA-seq, and Targeted Sequencing datasets to include somatic SNVs, InDels, CNVs, SVs, RNA expression, fusions, and splice variants. We integrated summarized CPTAC whole cell proteomics and phospho-proteomics data, miRNA-Seq data, and have developed a methylation array harmonization workflow to include m-values, beta-vales, and copy number calls. OpenPedCan contains reproducible, dockerized workflows in GitHub, CAVATICA, and Amazon Web Services (AWS) to deliver harmonized and processed data from over 60 scalable modules which can be leveraged both locally and on AWS. The processed data are released in a versioned manner and accessible through CAVATICA or AWS S3 download (from GitHub), and queryable through PedcBioPortal and the NCIs pediatric Molecular Targets Platform. Notably, we have expanded PBTA molecular subtyping to include methylation information to align with the WHO 2021 Central Nervous System Tumor classifications, allowing us to create research-grade integrated diagnoses for these tumors. ConclusionsOpenPedCan data and its reproducible analysis module framework are openly available and can be utilized and/or adapted by researchers to accelerate discovery, validation, and clinical translation.

genomics↗

BLADE-ON-PETIOLE interacts with CYCLOIDEA to fine-tune CYCLOIDEA-mediated flower symmetry in Monkeyflowers (Mimulus)

AbstractMorphological novelties, or key innovations, are instrumental to the diversification of the organisms. In plants, one such innovation is the evolution of zygomorphic flowers, which is thought to promote outcrossing and increases flower morphological diversity. We isolated three allelic mutants from two Mimulus species displaying altered floral symmetry and identified the causal gene as the orthologue of Arabidopsis BLADE-ON-PETIOLE. We found that MlBOP and MlCYC2a physically interact and this BOP-CYC interaction module is highly conserved across the angiosperms. Furthermore, MlBOP self-ubiquitinates and suppresses MlCYC2a self- activation. MlCYC2a, in turn, impedes MlBOP ubiquitination. Thus, this molecular tug-of-war between MlBOP and MlCYC2a fine-tunes the expression of MlCYC2a, contributing to the formation of bilateral symmetry flowers, a key trait in angiosperm evolution. One Sentence SummaryMolecular tug-of-war between MlBOP and MlCYC2a fine-tunes the expression of MlCYC2a, contributing to the bilateral flower symmetry formation.

developmental biology↗

AutoGVP: a dockerized workflow integrating ClinVar and InterVar germline sequence variant classification

SummaryWith the increasing rates of exome and whole genome sequencing, the ability to classify large sets of germline sequencing variants using up-to-date American College of Medical Genetics - Association for Molecular Pathology (ACMG-AMP) criteria is crucial. Here, we present Automated Germline Variant Pathogenicity (AutoGVP), a tool that integrates germline variant pathogenicity annotations from ClinVar and sequence variant classifications from a modified version of InterVar (PVS1 strength adjustments, removal of PP5/BP6). This tool facilitates large-scale, clinically-focused classification of germline sequence variants in a research setting. Availability and ImplementationAutoGVP is an open-source dockerized workflow implemented in R and freely available on GitHub at https://github.com/diskin-lab-chop/AutoGVP.

bioinformatics↗

Data-driven optimization yielded a highly-efficient CRISPR/Cas9 system for gene editing in Arabidopsis

The CRISPR/Cas9 technology is widely used for plant gene editing. In Arabidopsis, the early CRISPR/Cas9 systems using constitutive promoters to drive Cas9 expression usually have low heritable mutation efficiencies in the T1 generation. Germ cell-specific or cell division-specific promoters, like EC1.2en-EC1.1p fusion, YAO and CDC45, have been used as alternatives to direct Cas9 expression, but the efficiency of getting nonchimeric mutations is still not high. To further improve gene editing efficiency, we used gene co-expression network analysis to identify NUC1 as a candidate promoter for driving Cas9 expression. NUC1 has expression patterns similar to YAO, but expresses at a much higher level. We constructed a CRISPR/Cas9 system pHY07 that uses the NUC1 promoter to drive Cas9 and carries the mCherry protein as a fluorescent marker for selecting transgenic seeds. Using this system to edit the GL2 gene, we obtained apparently nonchimeric mutations in 55% of the T1 transgenic plants. Among the Cas9-free T2 plants 99% harbored mutations that are stably inherited from the previous generation. Therefore, our system exhibited extremely high editing efficiency, and through fluorescent screening of transgenic seeds, it become easy to obtain Cas9-free and stable genetic mutants in the T2 generation.

plant biology↗

An Azapeptide Platform in Conjunction with Covalent Warheads to Uncover High-Potency Inhibitors for SARS-CoV-2 Main Protease

Main protease (MPro) of SARS-CoV-2, the viral pathogen of COVID-19, is a crucial nonstructural protein that plays a vital role in the replication and pathogenesis of the virus. Its protease function relies on three active site pockets to recognize P1, P2, and P4 amino acid residues in a substrate and a catalytic cysteine residue for catalysis. By converting the P1 C atom in an MPro substrate to nitrogen, we showed that a large variety of azapeptide inhibitors with covalent warheads targeting the MPro catalytic cysteine could be easily synthesized. Through the characterization of these inhibitors, we identified several highly potent MPro inhibitors. Specifically, one inhibitor, MPI89 that contained an aza-2,2-dichloroacetyl warhead, displayed a 10 nM EC50 value in inhibiting SARS-CoV-2 from infecting ACE2+ A549 cells and a selectivity index of 875. The crystallography analyses of MPro bound with 6 inhibitors, including MPI89, revealed that inhibitors used their covalent warheads to covalently engage the catalytic cysteine and the aza-amide carbonyl oxygen to bind to the oxyanion hole. MPI89 represents one of the most potent MPro inhibitors developed so far, suggesting that further exploration of the azapeptide platform and the aza-2,2-dichloroacetyl warhead is needed for the development of potent inhibitors for the SARS-CoV-2 MPro as therapeutics for COVID-19.

biochemistry↗

Coupling of Slack and NaV1.6 sensitizes Slack to quinidine blockade and guides anti-seizure strategy development

Quinidine has been used as an anticonvulsant to treat patients with KCNT1-related epilepsy by targeting gain-of-function KCNT1 pathogenic mutant variants. However, the detailed mechanism underlying quinidines blockade against KCNT1 (Slack) remains elusive. Here, we report a functional and physical coupling of the voltage-gated sodium channel NaV1.6 and Slack. NaV1.6 binds to and highly sensitizes Slack to quinidine blockade. Homozygous knockout of NaV1.6 reduces the sensitivity of native sodium-activated potassium currents to quinidine blockade. NaV1.6-mediated sensitization requires the involvement of NaV1.6s N-and C-termini binding to Slacks C-terminus, and is enhanced by transient sodium influx through NaV1.6. Moreover, disrupting the Slack-NaV1.6 interaction by viral expression of Slacks C-terminus can protect against SlackG269S-induced seizures in mice. These insights about a Slack-NaV1.6 complex challenge the traditional view of "Slack as an isolated target" for anti-epileptic drug discovery efforts, and can guide the development of innovative therapeutic strategies for KCNT1-related epilepsy. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=134 SRC="FIGDIR/small/532982v3_ufig1.gif" ALT="Figure 1"> View larger version (31K): org.highwire.dtl.DTLVardef@1127858org.highwire.dtl.DTLVardef@19ad9f4org.highwire.dtl.DTLVardef@15b5542org.highwire.dtl.DTLVardef@13a86b4_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗