Biology subjects

Kwon, H.

Publications and source records attributed to Kwon, H..

At least 37 records · Page 2Linked to original sources

bioRxiv2025

Linoleic acid metabolite, 13-S-hydroxyoctadecadienoic acid, suppresses cancer cell growth by inhibiting mTOR

Mechanistic target of rapamycin (mTOR) is a key protein kinase that integrates various internal and external signals to control biological events including cell growth. Whereas substantial efforts were made to elucidate protein subunits interacting with mTOR, endogenous metabolite-mTOR interactions remain largely unknown. Using affinity protein purification and mass spectrometry, we identified direct binding of mTOR to 13-S-hydroxyoctadecadienoic acid (13-S-HODE) which is an oxygenated metabolite of linoleic acid, a polyunsaturated essential fatty acid. Interaction of 13-S-HODE with the catalytic ATP-binding domain of mTOR prevented its kinase activity in an ATP-competitive manner. Furthermore, either 13-S-HODE treatment or expression of arachidonate 15-lipoxygenase (ALOX15), an enzyme responsible for 13-S-HODE production, reduced mTOR signaling, thereby suppressing the growth of cancer cells as well as tumor xenografts. Our results highlight the importance of 13-S-HODE serving as a tumor suppressive, mTOR-inhibiting metabolite that links polyunsaturated fatty acid metabolism and the mTOR signaling in controlling cancer cell growth.

biochemistry↗

bioRxiv2025

LDB1 regulates gene expression and chromatin structure in pluripotency and lineage differentiation

Chromatin organization is a pivotal factor in stem cell pluripotency and differentiation. However, the role of enhancer looping protein LDB1 in stem cells has not been explored. We generated Ldb1(-/-) embryonic stem cells (ESC) using CRISPR/Cas9 editing and observed a reduction in key stem cell factors SOX2 and KLF4 upon LDB1 loss. Embryoid bodies (EB) derived from Ldb1(-/-) ESC displayed reduced expression of lineage-specific markers and impaired ability to undergo terminal differentiation to erythroblasts. Differential gene expression, including of the Lin28-mediated self-renewal pathway genes, was observed between WT and Ldb1(-/-) ESC and EB but was most pronounced after differentiation to erythroblasts. LDB1 occupied super enhancers, including those of pluripotency genes, in ESC together with pluripotency factors. LDB1 loss resulted in globally decreased chromatin accessibility in ESC and EB. Conditional LDB1-deficient mice displayed reduced hematopoietic stem cell markers on bone marrow cells, and dysregulation of the Lin28 pathway. Thus, LDB1 function is critical for ESC and EB development and becomes progressively more important during differentiation to erythroblasts.

developmental biology↗

bioRxiv2024

A genome-wide CRISPR screen in Anopheles mosquito cells identifies essential genes and required components of clodronate liposome function

Anopheles mosquitoes are the sole vector of human malaria, the most burdensome vector-borne disease worldwide. Strategies aimed at reducing mosquito populations and limiting their ability to transmit disease show the most promise for disease control. Therefore, gaining an improved understanding of mosquito biology, and specifically that of the immune response, can aid efforts to develop new approaches that limit malaria transmission. Here, we use a genome-wide CRISPR screening approach for the first time in mosquito cells to identify essential genes in Anopheles and identify genes for which knockout confers resistance to clodronate liposomes, which have been widely used in mammals and arthropods to ablate immune cells. In the essential gene screen, we identified a set of 1280 Anopheles genes that are highly enriched for genes involved in fundamental cell processes. For the clodronate liposome screen, we identified several candidate resistance factors and confirm their roles in the uptake and processing of clodronate liposomes through in vivo validation in Anopheles gambiae, providing new mechanistic detail of phagolysosome formation and clodronate liposome function. In summary, we demonstrate the application of a genome-wide CRISPR knockout platform in a major malaria vector and the identification of genes that are important for fitness and immune-related processes.

genetics↗

bioRxiv2024

Impaired sleep-dependent memory consolidation predicted by reduced sleep spindles in Rolandic epilepsy

Background and ObjectivesSleep spindles are prominent thalamocortical brain oscillations during sleep that have been mechanistically linked to sleep-dependent memory consolidation in animal models and healthy controls. Sleep spindles are decreased in Rolandic epilepsy and related sleep-activated epileptic encephalopathies. We investigate the relationship between sleep spindle deficits and deficient sleep dependent memory consolidation in children with Rolandic epilepsy. MethodsIn this prospective case-control study, children were trained and tested on a validated probe of memory consolidation, the motor sequence task (MST). Sleep spindles were measured from high-density EEG during a 90-minute nap opportunity between MST training and testing using a validated automated detector. ResultsTwenty-three children with Rolandic epilepsy (14 with resolved disease), and 19 age- and sex-matched controls were enrolled. Children with active Rolandic epilepsy had decreased memory consolidation compared to control children (p=0.001, mean percentage reduction: 25.7%, 95% CI [10.3, 41.2]%) and compared to children with resolved Rolandic epilepsy (p=0.007, mean percentage reduction: 21.9%, 95% CI [6.2, 37.6]%). Children with active Rolandic epilepsy had decreased sleep spindle rates in the centrotemporal region compared to controls (p=0.008, mean decrease 2.5 spindles/min, 95% CI [0.7, 4.4] spindles/min). Spindle rate positively predicted sleep-dependent memory consolidation (p=0.004, mean MST improvement of 3.9%, 95% CI [1.3, 6.4]%, for each unit increase in spindles per minute). DiscussionChildren with Rolandic epilepsy have a sleep spindle deficit during the active period of disease which predicts deficits in sleep dependent memory consolidation. This finding provides a mechanism and noninvasive biomarker to aid diagnosis and therapeutic discovery for cognitive dysfunction in Rolandic epilepsy and related sleep activated epilepsy syndromes.

neuroscience↗

bioRxiv2024

TNF signaling mediates cellular immune function and promotes malaria parasite killing in the mosquito Anopheles gambiae

Tumor Necrosis Factor- (TNF-) is a proinflammatory cytokine and a master regulator of immune cell function in vertebrates. While previous studies have implicated TNF signaling in invertebrate immunity, the roles of TNF in mosquito innate immunity and vector competence have yet to be explored. Herein, we confirm the identification of a conserved TNF- pathway in Anopheles gambiae consisting of the TNF- ligand, Eiger, and its cognate receptors Wengen and Grindelwald. Through gene expression analysis, RNAi, and in vivo injection of recombinant TNF-, we provide direct evidence for the requirement of TNF signaling in regulating mosquito immune cell function by promoting granulocyte midgut attachment, increased granulocyte abundance, and oenocytoid rupture. Moreover, our data demonstrate that TNF signaling is an integral component of anti-Plasmodium immunity that limits malaria parasite survival. Together, our data support the existence of a highly conserved TNF signaling pathway in mosquitoes that mediates cellular immunity and influences Plasmodium infection outcomes, offering potential new approaches to interfere with malaria transmission by targeting the mosquito host.

immunology↗

bioRxiv2024

In vivo Auto-tuning of Antibody-Drug Conjugate Delivery for Effective Immunotherapy using High-Avidity, Low-Affinity Antibodies

Antibody-drug conjugates (ADCs) have experienced a surge in clinical approvals in the past five years. Despite this success, a major limitation to ADC efficacy in solid tumors is poor tumor penetration, which leaves many cancer cells untargeted. Increasing antibody doses or co-administering ADC with an unconjugated antibody can improve tumor penetration and increase efficacy when target receptor expression is high. However, it can also reduce efficacy in low-expression tumors where ADC delivery is limited by cellular uptake. This creates an intrinsic problem because many patients express different levels of target between tumors and even within the same tumor. Here, we generated High-Avidity, Low-Affinity (HALA) antibodies that can automatically tune the cellular ADC delivery to match the local expression level. Using HER2 ADCs as a model, HALA antibodies were identified with the desired HER2 expression-dependent competitive binding with ADCs in vitro. Multi-scale distribution of trastuzumab emtansine and trastuzumab deruxtecan co-administered with the HALA antibody were analyzed in vivo, revealing that the HALA antibody increased ADC tumor penetration in high-expression systems with minimal reduction in ADC uptake in low-expression tumors. This translated to greater ADC efficacy in immunodeficient mouse models across a range of HER2 expression levels. Furthermore, Fc-enhanced HALA antibodies showed improved Fc-effector function at both high and low expression levels and elicited a strong response in an immunocompetent mouse model. These results demonstrate that HALA antibodies can expand treatment ranges beyond high expression targets and leverage strong immune responses.

bioengineering↗

bioRxiv2024

Mosquito immune cells enhance dengue and Zika virus dissemination in Aedes aegypti

Mosquito-borne viruses cause more than 400 million annual infections and place over half of the worlds population at risk. Despite this importance, the mechanisms by which arboviruses infect the mosquito host and disseminate to tissues required for transmission are not well understood. Here, we provide evidence that mosquito immune cells, known as hemocytes, play an integral role in the dissemination of dengue virus (DENV) and Zika virus (ZIKV) in the mosquito Aedes aegypti. We establish that phagocytic hemocytes are a focal point for virus infection and demonstrate that these immune cell populations facilitate virus dissemination to the ovaries and salivary glands. Additional transfer experiments confirm that virus-infected hemocytes confer a virus infection to non-infected mosquitoes more efficiently than free virus in acellular hemolymph, revealing that hemocytes are an important tropism to enhance virus dissemination in the mosquito host. These data support a "trojan horse" model of virus dissemination where infected hemocytes transport virus through the hemolymph to deliver virus to mosquito tissues required for transmission and parallels vertebrate systems where immune cell populations promote virus dissemination to secondary sites of infection. In summary, this study significantly advances our understanding of virus infection dynamics in mosquitoes and highlights conserved roles of immune cells in virus dissemination across vertebrate and invertebrate systems.

microbiology↗

bioRxiv2023

Metabolic and behavioral alterations associated with viral vector-mediated toxicity in the paraventricular hypothalamic nucleus

ObjectiveCombining adeno-associated virus (AAV)-mediated expression of Cre recombinase with genetically modified floxed animals is a powerful approach for assaying the functional role of genes in regulating behavior and metabolism. Extensive research in diverse cell types and tissues using AAV-Cre has shown it can save time and avoid developmental compensation as compared to using Cre driver mouse line crossings. We initially sought to study the impact of ablation of corticotropin-releasing hormone (CRH) in the paraventricular hypothalamic nucleus (PVN) using intracranial AAV-Cre injection in adult animals. MethodsIn this study, we stereotactically injected AAV8-hSyn-Cre or a control AAV8-hSyn-GFP both Crh-floxed and wild-type mouse PVN to assess behavioral and metabolic impacts. We then used immunohistochemical markers to systematically evaluate the density of hypothalamic peptidergic neurons and glial cells. ResultsWe found that delivery of one specific preparation of AAV8-hSyn-Cre in the PVN led to the development of obesity, hyperphagia, and anxiety-like behaviors. This effect occurred independent of sex and in both floxed and wild-type mice. We subsequently found that AAV8-hSyn-Cre led to neuronal cell death and gliosis at the site of viral vector injections. These behavioral and metabolic deficits were dependent on injection into the PVN. An alternatively sourced AAV-Cre did not reproduce the same results. ConclusionsOur findings reveal that delivery of a specific batch of AAV-Cre could lead to cellular toxicity and lesions in the PVN that cause robust metabolic and behavioral impacts. These alterations can complicate the interpretation of Cre-mediated gene knockout and highlight the need for rigorous controls.

neuroscience↗

bioRxiv2023

Characterising the Protein-Protein Interaction Between MDM2 and 14-3-3σ; Proof of Concept for Small Molecule Stabilisation

Mouse Double Minute 2 (MDM2) is a key negative regulator of the tumour suppressor protein p53. MDM2 overexpression occurs in many types of cancer and results in the suppression of wild type p53. The 14-3-3 family of adaptor proteins are known to bind to MDM2 and the 14-3-3{sigma} isoform controls MDM2 cellular localisation and stability to inhibit its activity. Therefore, small molecule stabilisation of the 14-3-3{sigma}/MDM2 protein-protein interaction (PPI) is a potential therapeutic strategy for the treatment of cancer. In this work we provide a detailed biophysical and structural characterisation of the phosphorylation-dependent interaction between 14-3-3{sigma} and peptides that mimic the 14-3-3 binding motifs within MDM2. The data show that di-phosphorylation of MDM2 at S166 and S186 is essential for high affinity 14-3-3 binding and that the binary complex formed involves one MDM2 di-phosphorylated peptide bound to a dimer of 14-3-3{sigma}. Each of the two phosphorylated stretches of MDM2 occupies one of the two binding grooves of a 14-3-3{sigma} dimer, a novel model for binding of di-phosphorylated peptides to 14-3-3 proteins. In addition, we show that the 14-3-3{sigma}/MDM2 interaction is amenable to small molecule stabilisation. The natural product fusicoccin A forms a ternary complex with a 14-3-3{sigma} dimer and an MDM2 di-phosphorylated peptide resulting in stablisation of the 14-3-3{sigma}/MDM2 PPI. This work serves as a proof-of-concept of the drugability of the 14-3-3/MDM2 PPI and paves the way toward the development of more selective and efficacious small molecule stabilisers.

biochemistry↗

bioRxiv2023

Monomeric amyloid-β inhibits microglial inflammatory activity in the brain via an APP/heterotrimeric G protein-mediated pathway

Microglia, the resident immune cell of the brain, play critical roles in brain development, function, and disease. However, how microglial activity is regulated in this process remains to be elucidated. Here we report an amyloid precursor protein (APP) and heterotrimeric G protein-mediated pathway that negatively regulates microglial inflammatory activation during cerebral cortex development. Disruption of this pathway results in dysregulated microglial activity, excessive extracellular matrix proteinase production, cortical basement membrane breach, and laminar assembly disruption. We further show that this pathway is activated by amyloid {beta} (A{beta}), the cleavage product of APP that accumulates in large quantities as plaques in the Alzheimers disease brain. Specifically, we find A{beta} monomers potently suppress inflammatory cytokine transcription and secretion by brain microglia, in an APP and heterotrimeric G protein-dependent manner. These results discover a previously unknown activity of A{beta} as a negative regulator of brain microglia as well as a new pathway that mediates the signal transduction. They shed new light on the cell-cell communication mechanisms that regulate brain immune homeostasis and may facilitate further insight into Alzheimers disease pathogenesis.

neuroscience↗

bioRxiv2023

Preliminary evidence of a relationship between sleep spindles and treatment response in epileptic encephalopathy

ObjectiveEpileptic encephalopathy with spike wave activation in sleep (EE-SWAS) is a challenging neurodevelopmental disease characterized by abundant epileptiform spikes during non-rapid eye movement (NREM) sleep accompanied by cognitive dysfunction. The mechanism of cognitive dysfunction is unknown, but treatment with high-dose diazepam may improve symptoms. Spike rate does not predict treatment response, but spikes may disrupt sleep spindles. We hypothesized that in patients with EE-SWAS: 1) spikes and spindles would be anticorrelated, 2) high-dose diazepam would increase spindles and decrease spikes, and 3) spindle response would be greater in those with cognitive improvement. MethodsConsecutive EE-SWAS patients treated with high-dose diazepam that met criteria were included. Using a validated automated spindle detector, spindle rate, duration, and percentage were computed in pre- and post-treatment NREM sleep. Spikes were quantified using a validated automated spike detector. Cognitive response was determined from chart review. ResultsSpindle rate was anticorrelated with spike rate in the channel with the maximal spike rate (p=0.002) and averaged across all channels (p=0.0005). Spindle rate, duration, and percentage each increased, and spike rate decreased, after high-dose diazepam treatment (p[≤]2e-5, all tests). Spindle rate, duration, and percentage (p[≤]0.004, all tests) were increased in patients with cognitive improvement after treatment, but not those without. Changes in spike rate did not distinguish between groups. InterpretationThese findings confirm thalamocortical disruption in EE-SWAS, identify a mechanism through which benzodiazepines may support cognitive recovery, and introduce sleep spindles as a promising mechanistic biomarker to detect treatment response in severe epileptic encephalopathies.

neuroscience↗

bioRxiv2023

The neural activity of auditory conscious perception

Although recent work has made significant headway in understanding the temporal and spatial dynamics of the neural mechanisms of conscious perception, much of that work has focused on visual paradigms. To determine whether there are shared mechanisms for perceptual consciousness across sensory modalities, here we developed a task to test within the auditory domain. Participants (n=31) completed an auditory perceptual threshold task while undergoing intracranial electroencephalography (icEEG) for intractable epilepsy. Intracranial recordings from over 2,800 grey matter electrodes representing widespread cortical coverage were analyzed for power in the high gamma range (40-115 Hz)--a frequency range that reflects local neural activity. For trials that were perceived, we find activity in early auditory regions which is accompanied by activity in the right caudal middle frontal gyrus, and shortly thereafter by activity in non-auditory thalamus. This is followed by a wave of activity that sweeps through the higher auditory association regions and into parietal and frontal cortices, similar to the wave observed in our visual conscious perception paradigm. However, for not perceived trials, we find that significant activity is restricted to early auditory regions (and areas immediately adjacent to the Sylvian fissure). These findings show that the broad anatomical regions of cortical and subcortical networks involved in auditory perception are similar to the networks observed with vision, suggesting shared general mechanisms for conscious perception.

neuroscience↗

bioRxiv2022

Extracellular vesicles secreted by Brugia malayi microfilariae modulate the melanization pathway in the mosquito host

Vector-borne, filarial nematode diseases represent a significant and affecting disease burden in humans, domestic animals, and livestock worldwide. Parasitic filarial nematodes require both an intermediate (vector) host and a definitive (mammalian) host during the course of their life cycle. In either host, the nematode must evade the host elicited immune response in order to develop and establish infection. There is direct evidence of parasite-derived immunomodulation in mammals, however, there is less evidence of parasite immunomodulation of the vector host. We have previously reported that all life stages of Brugia malayi, a causative agent of lymphatic filariasis, secrete extracellular vesicles (EVs). Here we investigate the immunomodulatory effects of microfilariae derived EVs on the vector host Aedes aegypti. RNA-seq analysis of an A. aegypti cell line treated with B. malayi microfilariae EVs showed differential expression of both mRNAs and miRNAs, some with roles in immune regulation. One downregulated gene, AAEL002590, identified as a serine protease, was shown to have direct involvement in the phenoloxidase (PO) cascade through analysis of PO activity. Similarly, injection of adult female mosquitoes with B. malayi microfilariae EVs validated these results in vivo, eliciting a downregulation of the AAEL002590 transcript and a significant reduction in PO activity. Our data indicates that parasite-derived EVs are capable of interfering with critical immune responses in the vector host, particularly immune responses such as melanization that target extracellular parasites. In addition, this data provides novel targets for transmission control strategies for LF and other parasitic diseases. Author SummaryVector-borne, filarial nematode diseases represent a significant and affecting disease burden in humans, domestic animals and livestock worldwide. Parasitic nematodes must evade the elicited immune response of their hosts in order to develop and establish infection. While there is evidence for immunomodulation of the mammalian host, the mechanism of this immunomodulation is not fully clear and there is limited evidence for immunomodulation of the vector host. Here we have shown that parasite-derived extracellular vesicles are effector structures for immunomodulation of the vector host. In particular, we have identified that parasite-derived extracellular vesicles can interfere with critical mosquito immune responses against parasites. This data provides insight into parasite biology and novel targets for transmission control strategies for parasitic diseases.

immunology↗

bioRxiv2022

Normative sleep spindle database and findings from 772 healthy children from birth through 18 years

Work in the last two decades has identified sleep spindles, discrete "sigma band" oscillations during stage 2 sleep, as a key oscillatory mechanism required for off-line memory consolidation. Although, sleep spindles are known to evolve concomitant with brain maturation and reflect cognitive function across the lifespan, the details of this developmental trajectory are unknown. To address this, we curated a database of sleep electroencephalograms from 772 developmentally normal children to characterize spindles from birth through 18 years. After validating an automated spindle detector against ~20,000 hand-marked spindles across ages, we demonstrate that sleep spindle features follow distinct age-specific patterns in distribution, rate, duration, frequency, estimated refractory period, and inter-hemispheric spindle lag. These data expand our current knowledge of normal physiological brain development and provide a large normative database to detect deviations in sleep spindles to aid discovery, biomarker development, and diagnosis in pediatric neurodevelopmental disorders.

neuroscience↗

bioRxiv2021

Early neural activity changes associated with visual conscious perception

The neural mechanisms of visual conscious perception have been investigated for decades. However, the spatiotemporal dynamics associated with the earliest neural responses following consciously perceived stimuli are still poorly understood. Using a dataset of intracranial EEG recordings, the current study aims to investigate the neural activity changes associated with the earliest stages of visual conscious perception. Subjects (N=10, 1,693 grey matter electrode contacts) completed a continuous performance task in which individual letters were presented in series and subjects were asked to press a button when they saw a target letter. Broadband gamma power (40-115Hz) dynamics were analyzed in comparison to baseline prior to stimulus and contrasted for target trials with button presses and non-target trials without button presses. Regardless of event type, we observed early gamma power changes within 30-150 ms from stimulus onset in a network including increases in bilateral occipital, fusiform, frontal (including frontal eye fields), and medial temporal cortex, increases in left lateral parietal-temporal cortex, and decreases in the right anterior medial occipital cortex. No significant differences were observed between target and non-target stimuli until >150 ms post-stimulus, when we saw greater gamma power increases in left motor and premotor areas, suggesting a possible role of these later signals in perceptual decision making and/or motor responses with the right hand. The early gamma power findings suggest a broadly distributed cortical visual detection network that is engaged at early times tens of milliseconds after signal transduction from the retina.

neuroscience↗

bioRxiv2021

Fast volumetric imaging with line-scan confocal microscopy by an electro-tunable lens

In microscopic imaging of biological tissues, particularly real-time visualization of neuronal activities, rapid acquisition of volumetric images poses a prominent challenge. Typically, two-dimensional (2D) microscopy can be devised into an imaging system with 3D capability using any varifocal lens. Despite the conceptual simplicity, such an upgrade yet requires additional, complicated device components and suffers a reduced acquisition rate, which is critical to document neuronal dynamics properly. In this study, we implemented an electro-tunable lens (ETL) in the line-scan confocal microscopy, enabling the volumetric acquisition at the rate of 20 frames per second with the maximum volume of interest of 315 x 315 x 80 m3. The axial extent of point-spread-function (PSF) was 17.6 {+/-} 1.6 m and 90.4 {+/-} 2.1 m with the ETL operating in either stationary or resonant mode, respectively, revealing significant depth elongation by the resonant mode ETL microscopy. We further demonstrated the utilities of the ETL system by volume imaging of cleared mouse brain ex vivo samples and in vivo brains. The current study foregrounds the successful application of resonant ETL for constructing a basis for a high-performance 3D line-scan confocal microscopy system, which will enhance our understanding of various dynamic biological processes.

bioengineering↗

bioRxiv2021

Tagging active neurons by soma-targeted Cal-Light

Verifying causal effects of neural circuits is essential for proving direct a circuit-behavior relationship. However, techniques for tagging only active neurons with high spatiotemporal precision remain at the beginning stages. Here we developed the soma-targeted Cal-Light (ST-Cal-Light) which selectively converts somatic calcium rise triggered by action potentials into gene expression. Such modification simultaneously increases the signal-to-noise ratio (SNR) of reporter gene expression and reduces the light requirement for successful labeling. Because of the enhanced efficacy, the ST-Cal-Light enables the tagging of functionally engaged neurons in various forms of behaviors, including context-dependent fear conditioning, leverpressing choice behavior, and social interaction behaviors. We also targeted kainic acid-sensitive neuronal populations in the hippocampus which subsequently suppressed seizure symptoms, suggesting ST-Cal-Lights applicability in controlling disease-related neurons. Furthermore, the generation of a conditional ST-Cal-Light knock-in (KI) mouse provides an opportunity to tag active neurons in a region- or cell-type specific manner via crossing with other Cre-driver lines. Thus, the versatile ST-Cal-Light system links somatic action potentials to behaviors with high temporal precision, and ultimately allows functional circuit dissection at a single cell resolution.

neuroscience↗

bioRxiv2021

Brain networks in human conscious visual perception

Consciousness is not explained by a single mechanism, rather it involves multiple specialized neural systems overlapping in space and time. We hypothesize that synergistic, large-scale subcortical and cortical attention and signal processing networks encode conscious experiences. To identify brain activity in conscious perception without overt report, we classified visual stimuli as perceived or not using eye measurements. Report-independent event-related potentials and functional magnetic resonance imaging (fMRI) signals both occurred at early times after stimuli. Direct recordings revealed a novel thalamic awareness potential linked to conscious visual perception based on report. fMRI showed thalamic and cortical detection, arousal, attentional salience, task-positive, and default mode networks were involved independent of overt report. These findings identify a specific sequence of neural mechanisms in human conscious visual perception. One-Sentence SummaryHuman conscious visual perception engages large-scale subcortical and cortical networks even without overt report.

neuroscience↗