Biology subjects

Tian, R.

Publications and source records attributed to Tian, R..

At least 19 recordsLinked to original sources

bioRxiv2026

p53 activity links chromosomal instability to pro-migratory extracellular vesicles

Chromosomal instability (CIN) promotes tumor evolution and metastasis while imposing cellular stress that can limit cell proliferation via activation of p53 and its downstream effector p21. However, how cells recover from this p53-mediated proliferation block while adopting a more malignant fate remains poorly understood. Here, using a p21-RFP reporter in p53-proficient NIH/3T3 cells, we show that acute CIN gives rise to two phenotypically distinct p21 cell populations with divergent recovery trajectories. p21-RFPLOW cells re-enter the cell cycle following a short cell-cycle arrest, while p21-RFPHIGH cells display a more persistent arrest that coincides with a senescence-like state. Longitudinal transcriptomic and extracellular vesicle (EV) proteomic analyses reveal that extracellular-matrix (ECM)- and adhesion-associated programs are initially suppressed following CIN but specifically reactivated in p21-RFPHIGH cells. The content of late-stage p21-RFPHIGH-derived EVs is enriched for ECM-, adhesion-, and cytoskeleton-associated proteins compared with that of p21-RFPLOW-derived EVs. Consequently, EVs derived from p21-RFPHIGH cells confer increased migration. Together, these findings reveal that CIN can yield distinct p21-expressing cell populations that display different cell-cycle recovery trajectories, EV makeup, and migration-associated paracrine activity.

cancer biology↗

bioRxiv2026

An Integrated Atlas of the Human Kidney Spanning Health and Diseases

The human kidney contains highly specialized cell populations. Despite numerous single-cell and single-nucleus transcriptomics studies, differences in cohorts, technologies, analytical pipelines, and annotation frameworks have limited the ability to define consensus kidney cell states, identify disease-associated populations and interpret kidney disease genetic susceptibility. Here, we assembled 18 human kidney single-cell and single-nucleus RNA-sequencing datasets spanning 232 donors and five major disease contexts into a uniformly processed and computationally integrated Human Kidney Cell Atlas (HKCA), comprising over one million high-quality cells (816,895) and nuclei (215,308). The HKCA resolves 63 cell types and 120 harmonized cell states, including rare epithelial and stromal populations associated with kidney diseases . Integration with spatial transcriptomics, intercellular communication networks, and human genetic association data further defined the anatomical context and disease relevance of these populations. The HKCA also provides a framework for automated annotation of independent kidney human and mouse datasets. Together, the HKCA establishes a comprehensive reference for human kidney biology, enabling disease interpretation and genetic risk localization at cellular resolution.

genomics↗

bioRxiv2026

BaiZe: A Multi-View Dynamic Framework for Simulating and Interpreting Cellular Responses Across Perturbation Contexts

Accurately predicting how cells respond to perturbations is important for understanding cellular regulation and prioritizing experimental interventions, yet existing models are often designed for specific perturbation types or biological contexts. Here we present BaiZe, a multi-view conditional state-transition framework that predicts the post-perturbation transcriptome from a control-state transcriptome together with genetic, chemical, temporal and optional chromatin-accessibility information. BaiZe models perturbation responses as context-dependent transitions between cellular states. BaiZe supports prediction across held-out cell states and genetic perturbations, unseen multi-gene combinations, chemical structures and doses, temporal stages and species contexts. Benchmarking across diverse perturbation settings demonstrates that BaiZe effectively recovers major transcriptional response programs under previously unseen conditions. Incorporating matched ATAC-seq context further improves selected state-transition predictions and enables model-based attribution of chromatin regions to response-associated genes and pathways. BaiZe also supports few-shot transfer of perturbation responses from human to mouse cellular systems and connects predicted transcriptomes to candidate morphology projections. To facilitate interpretation and use, BaiZe-Agent organizes response genes, pathways, chromatin evidence, cross-species predictions and projected phenotypes into traceable, queryable perturbation records. Together, BaiZe provides a broadly applicable framework for predicting and interpreting context-dependent cellular responses and for prioritizing hypotheses across diverse perturbation settings.

bioinformatics↗

bioRxiv2026

Psilocybin Attenuates Cortical Representations of Aversion in the Mouse Auditory Cortex

Psilocybin can produce sustained benefits in affective and trauma-related disorders, yet if and how it reshapes sensory representations of learned valence associations remains largely unclear. To address this, we used longitudinal two-photon calcium imaging in awake C57BL/6 mice to examine how psilocybin modulates layer 2/3 auditory cortex activity at single-cell and population levels. Evoked responses were measured for tones with or without prior associations with valenced stimuli, as well as for the valenced stimuli themselves. Most responsive neurons were selective for tones alone, while distinct subsets responded exclusively to reward or aversive stimuli, and a smaller population encoded both. Psilocybin selectively reduced responses to aversive stimuli and earlier-established aversive-associated tones, without affecting aversive association, reward responses, or responses to newly aversive-associated tones. At the population level, psilocybin acutely increased coordination across tone-responsive neurons, while later reducing it selectively among neurons encoding the aversive-associated tone. These results demonstrate that psilocybin preferentially dampens well consolidated aversive sensory representations in auditory cortex, rather than fresh associations, without broadly affecting auditory processing or new aversive learning.

neuroscience↗

bioRxiv2026

Coronavirus envelope protein drives iron sensing disorder by hijacking the TAp73-FDXR axis

Iron overload is increasingly recognized as a critical contributor to coronavirus pathogenesis1, yet the underlying induction mechanisms remain unclear. Here, we uncover a fundamental pathway by which coronavirus drives IRP1 RNA-binding activity to induce iron accumulation2 via targeting the TAp73-FDXR axis. Specifically, coronavirus infection represses transcription of FDXR (encoding the key rate-limiting enzyme in host iron-sulfur cluster synthesis3), thereby impairing host iron-sulfur cluster generation to trigger the functional conversion of the cytosolic aconitase 1 (ACO1) into iron-regulatory protein 1 (IRP1)4, ultimately leading to the hosts persistently false perception of iron deficiency. We identify TAp73 as the primary transcription factor governing FDXR expression, and demonstrate that the coronavirus envelope protein (CoV-E) orchestrates TAp73 nuclear export. Subsequently, CoV-E binds TAp73 through a critical valine residue within its C-terminal PBM domain, inducing the K48-linked ubiquitination and proteasomal degradation of TAp73. Furthermore, we developed a CoV-E-targeting molecule, DPTP-FC, which blocks CoV-E-TAp73 interaction via forming steric hindrance and effectively alleviates iron accumulation and tissue damage caused by PEDV, PDCoV, and SARS-CoV-2 infection. Our study reveals the central role of the TAp73-FDXR axis in CoV-induced iron accumulation, highlighting CoV-E as an attractive antiviral target and DPTP-FC as a promising therapeutic candidate.

microbiology↗

bioRxiv2026

A Grass-Specific Structural Feature of Myosin VIII Regulates Protoxylem Development and Hydraulic Conductance in Sorghum

Sorghum (Sorghum bicolor), a C grass adapted to hot semi-arid environments, depends on reinforced xylem vessels to maintain hydraulic conductance under high evaporative demand. During protoxylem differentiation, coordinated microtubule and actin dynamics guide secondary cell wall (SCW) deposition; however, whether actin-based motors directly regulate vascular architecture and hydraulic performance has remained unknown. Here, we identify HEAT-SENSITIVE 1 (HS1), a previously uncharacterized myosin VIII, as a central regulator of protoxylem integrity and water transport in sorghum. The hs1 mutant exhibited severe leaf scorching under field conditions. The hs1 mutant displayed severe leaf scorching under field conditions, accompanied by pronounced protoxylem defects under controlled environments, including vessel collapse, reduced lumen area, and attenuated lignified SCWs. These structural abnormalities compromised longitudinal hydraulic conductance, diminished whole-plant water use, and rendered expanding leaves unable to meet transpirational demand, resulting in transient water deficit and thermal injury. HS1 encoded a grass-specific myosin VIII with a grass-specific N-terminal extension exhibiting high intrinsic disorder and lineage-specific substitutions in the motor domain. Molecular and single-cell transcriptome analyses positioned HS1 within differentiating protoxylem cells of developing leaves, revealing pronounced temporal and cell-type specificity. Furthermore bulk transcriptome profiling and quantitative lignin measurements indicated that HS1 promoted lignin-associated SCW biosynthesis during protoxylem differentiation, functionally linking actin-based motor activity to wall reinforcement. HS1 encodes a grass-specific myosin VIII distinguished by an extended intrinsically disordered N-terminal region and lineage-specific substitutions within the motor domain, suggesting evolutionary specialization. Consistant with core developmental role, reduced nucleotide diversity at the HS1 locus across diverse sorghum accessions further supported strong evolutionary constraint. Together, these findings established HS1 as the first actin-based motor protein shown to control xylem architecture and hydraulic function in plants.

plant biology↗

bioRxiv2026

A portable orthogonal replication system enables continuous gene evolution near the biological speed limit

Orthogonal DNA replication systems uncouple the mutagenesis of target genes from host viability, enabling target gene hypermutation beyond the genomic critical error threshold and thereby unlocking access to greater sequence space for accelerated evolution. Here we introduce a series of upgrades to the E. coli orthogonal replication system, EcORep. We develop strategies to efficiently establish, engineer, and transform orthogonal replicons. We develop and utilize replicon-REXER to establish a 77 kb replicon, the largest orthogonal replicon reported to date. Directed evolution of the orthogonal DNA polymerase yielded variants with mutation rates of [~]10-4 substitutions per base per generation and best-in-class mutational spectra. These polymerases are three orders of magnitude more mutagenic than the first-generation EcORep system, enable mutagenesis at one million times the genomic levels, and straddle the evolutionary critical error threshold for the mutation of genes tested. Using the highly mutagenic EcORep system, we rapidly evolve an ethanol assimilation pathway for increased performance. Furthermore, we find that the three components sufficient to drive the minimal EcORep system enable O-replication systems to be established in other Gram-negative bacteria. Thus, we establish VinORep in Vibrio natriegens. VinORep combines O-replicon mutation, around the limit for molecular evolution of genes, with the fastest growing organism, to realize gene evolution approaching the biological speed limit. We exemplify the utility of this advance through the rapid evolution of new function - via the accumulation of tens of mutations, and selection - in 16 hours.

synthetic biology↗

bioRxiv2026

Pollutant biodegradation profile mediated by multi-trophic microbial dynamics in rivers

Microbial communities and environmental conditions are closely linked to ecosystem functions and directly govern the biodegradation of pollutants in aquatic environments. However, the role of multi-trophic interactions and their spatiotemporal dynamics in these processes remains poorly understood. Here, we examined how seasonal and spatial variations, mediated by trophic interactions within benthic microbial communities, influence their composition, functional capacity, and collective potential to degrade a diverse array of organic pollutants in rivers. By characterizing both prokaryotic (i.e., archaea and bacteria) and eukaryotic taxa (i.e., algae, fungi, protists, and metazoans), and inferring metabolic pathways, we explored the connections between community composition and pollutant degradation in wastewater-receiving rivers across four seasons. Mediation analysis revealed that multi-trophic communities mediate the total effect of environmental factors on the biodegradation of 96 organic pollutants. Prokaryotic communities explained 60% of the total environmental influence on pollutant biodegradation. Additionally, eukaryotic groups had significant indirect mediation effects, with fungal, protistan, algal, and metazoan communities responsible for 56%, 53%, 26%, and 38%, respectively. Notably, fungal and protist communities mediated approximately 83% and 73% of the environmental impacts on prokaryotic community composition, respectively. Across the two rivers studied, spatial variation (at the river and reach scales) explained more variance in community composition than seasonality over the sampled year. Our findings improve understanding of ecosystem resilience and support the development of predictive models and sustainable water management strategies in dynamic aquatic environments.

microbiology↗

bioRxiv2026

AutoPELSA: an automated sample preparation system for proteome-wide identification of target proteins of diverse ligands

Protein-ligand interactions are fundamental to cellular function and drug discovery, and ligand-modification-free strategies have emerged as powerful tools for proteome-wide interrogation of these interactions. Among these, the peptide-centric local stability assay (PELSA) stands out for its high sensitivity. It uses a single digestion step to detect ligand-induced local stability shifts, enabling precise binding region localization and affinity estimation. However, manual PELSA workflows suffer from multiple labor-intensive steps that introduce variability and constrain throughput, limiting large-scale applications. To address these limitations, we developed AutoPELSA, an automated platform that streamlines the PELSA workflow including the limited proteolysis step and the following peptide separation step. AutoPELSA completes 96 samples in [~]4 h, enabling high-throughput analysis under native conditions. AutoPELSA reliably detected targets of both strong-affinity ligands (e.g., staurosporine, identifying 114 kinase targets) and low-affinity ligands, including -ketoglutarate (30 known targets). Furthermore, a mixed-ligand dose-response strategy enabled simultaneous determination of binding affinities for multiple ligand-protein interaction regions in a single experiment. Overall, AutoPELSA provides a scalable and modification-free platform for proteome-wide identification and affinity profiling of ligand-protein interactions.

molecular biology↗

bioRxiv2025

CaRPOOL: A Pooled Calcium-Recording CRISPR Screening Platform Identifies CCR7 as a Modulator of Cellular Osmomechanosensing

Cells must continuously sense and respond to environmental changes by translating physical and chemical cues into intracellular signals. However, systematic discovery of genes governing these sensory processes has been limited by the transient nature of signaling events and the low throughput of measurement assays. Here, we present CaRPOOL, a pooled, high-throughput genetic screening platform that integrates the calcium-activity recorder CaMPARI2 with CRISPR interference (CRISPRi), enabling stable capture of transient calcium signals for genome-scale functional screening. Using osmomechanical stimulation as a model, we demonstrate that CaMPARI2 photoconversion faithfully reports stimulus-dependent calcium responses and supports pooled fluorescence-activated cell sorting (FACS)-based screening. A CRISPRi library targeting membrane-associated genes identified both known and previously uncharacterized regulators of mechanotransduction, including the chemokine receptor CCR7. Mechanistic analyses revealed that CCR7 promotes osmomechanical calcium signaling through a PIEZO1-dependent Gs-cAMP-PKA pathway, establishing it as a mechanically responsive GPCR. Notably, osmotic stress upregulated CCR7 expression in immune cell lines and enhanced mechanical responsiveness, suggesting a role in immunomechanical adaptation. Together, these findings introduce a broadly applicable platform for high-throughput discovery of genes controlling dynamic signaling responses and reveal a GPCR-ion channel crosstalk mechanism in mechanotransduction with potential implications for immune cell mechanoadaptation.

cell biology↗

bioRxiv2025

Integrative metabolome-genome analysis reveals the genetic architecture of metabolic diversity in sorghum grain

Natural variation in the grain metabolome plays a central role in shaping nutritional quality and end-use traits in grass crops. Understanding the genetic basis of this metabolic diversity is therefore essential, yet population-scale integration of metabolomics and genomics remains limited in sorghum, a climate-resilient C4 crop renowned for its exceptional heat and drought tolerance. Here, we integrated large-scale untargeted metabolomic profiling, population genomics, and artificial intelligence (AI)-based machine learning to systematically dissect grain metabolic diversity and its genetic architecture in sorghum. Untargeted metabolomic profiling of mature grains of the Sorghum Association Panel (SAP) identified 4,877 compounds, revealing extensive quantitative variation relevant to grain nutritional improvement. Metabolite-based genome-wide association studies (mGWAS) identified [~]4.15 million significant SNP-metabolite associations, revealing the heterogeneous genetic architecture of metabolic traits. Associated variants were enriched in genic and regulatory regions but depleted in intergenic regions, consistent with functional constraint. A total of 38 metabolite gene clusters revealed coordinated genetic control of core metabolic pathways. We further applied machine learning to identify key metabolites that underlie grain color variation and to prioritize associated candidate genes, demonstrating the utility of predictive models integrating genotype, metabolome, and end trait. Collectively, this work establishes a population-scale atlas of sorghum grain metabolomic and genetic diversity, available through the Sorghum Grain Metabolite Diversity Atlas (SorGMDA). This resource enables integrated metabolomics and genomic analyses and supports systems-level breeding strategies for improving grain nutritional quality.

genomics↗

bioRxiv2025

Lysine-R2HGylation identified as a post-translational modification in R2HG-elevated cancers

R-2-Hydroxyglutarate (R2HG), an oncometabolite predominantly produced by mutated isocitrate dehydrogenase 1/2 (IDH1/2) in various cancers, is known to drive cancer progression through noncovalent inhibition of -ketoglutarate (KG)-dependent enzymes. In this work, we propose an alternative mechanism wherein R2HG contributes to cancer development via covalent modification of biologically critical lysines, a process termed lysine-R2HGylation (KR2HG). We designed and synthesized R2HG-mimicking probes, demonstrating their effectiveness in facilitating KR2HG target profiling and site mapping. We identified KR2HG as a previously unrecognized post-translational modification, confirmed its C5-linkage on GSTP1(K209), and demonstrated that SIRT5 functions as a deacylase for GSTP1-KR2HG in vitro. Furthermore, we found that R2HG slightly but significantly inhibits the enzymatic activity of GSTP1 through KR2HG and dramatically suppresses monocyte differentiation via this catalytically important lysine modification. Our findings provide an alternative perspective on the role of R2HG in leukemia progression and offer a practical tool for the clinical investigation of R2HG-elevated cancers.

molecular biology↗

bioRxiv2025

Poising and connectivity of emergent human developmental enhancers in the transition from naive to primed pluripotency

In primed human pluripotent stem cells (hPSCs) resembling post-implantation epiblast, numerous lineage-specific enhancers assume the poised chromatin state, co-marked by H3K4me1 and Polycomb-associated H3K27me3 histone modifications. In contrast, poised enhancers (PEs) are scarce in naive hPSCs that model pre-implantation epiblast. PEs form abundant chromosomal contacts with developmental genes, but when these contacts emerge, how their formation relates to enhancer poising and their functional significance remains incompletely understood. Here, we devise high-resolution, PE-targeted Capture Hi-C to generate a comprehensive atlas of PE chromosomal contacts in the time course of hPSC transition from the naive to primed state. We find that enhancer poising emerges early in the transition, while the contacts show diverse dynamics that is only partially coupled to poising. PROTAC-induced degradation of Polycomb Repressive Complex 2 (PRC2) early in the transition weakens PE connectivity, while inhibition of its H3K27 methyltransferase activity does not, suggesting a non-catalytic role of Polycomb in supporting PE contacts. Notably, PE contacts persist after developmental activation or ectopic CRISPRa targeting and can mediate long-range gene induction. Together, these findings reveal the temporal and mechanistic principles of PE connectivity, highlighting a potential role of PE contacts in establishing gene expression patterns in human development.

genomics↗

bioRxiv2025

Evaluation of the nano Liquid Chromatography coupled with Zeno TOF 7600 Mass Spectrometer for Cell Type-Resolved Spatial Proteomics

In this study, we systematically evaluated the nanoLC-Zeno TOF platform using data-independent acquisition (DIA) and identified 3,142 to 7,059 protein groups from 1 to 200 ng of standard K562 digest. Additionally, a targeted acquisition strategy detected 184 peptides with enhanced signal using Zeno activation. To achieve spatial cell-type resolved proteomics, we developed a workflow integrating image-guided laser capture microdissection for analysis of gastric cancer tissue. A 30-minute nanoLC gradient facilitated the quantification of 2,514 proteins from 0.2 mm{superscript 2} regions representing cancer cells, cancer-associated fibroblasts (CAFs), and immune cells, as defined by multiplex immunohistochemistry. This spatial proteomics approach revealed cellular heterogeneity within the tumor microenvironment of a clinical gastric cancer sample, and targeted validation identified differential expression of 12 cancer-associated proteins comprising 103 peptides between cancer cell-enriched and CAFs-enriched regions. This workflow offers a practical strategy for spatial visual proteomic analysis in clinical tissue samples.

cancer biology↗

bioRxiv2025

Towards Unmanned Proteomics Data Generation: A Fully Automated Sample-to-Data System for Proteomic Experiments

The {pi}-HuB project requires proteomic measurements of millions of low-input samples that are challenging with current technology. Here, we introduce a pilot {pi}-HuB data factory that features a fully automated sample-to-data system to enable high-throughput digitization of human samples. Our platform, as a proof-of-concept towards unmanned proteomics, was demonstrated to show longitudinal robustness and applied for spatial proteomics and the profiling of plasma and cell lines, thereby serving as the workhorse to drive {pi}-HuB.

biochemistry↗

bioRxiv2025

The XPF-like domain in SHOC1 required for homologous recombination and safeguarding autosome from meiotic silencing of unsynapsed chromatin

During meiosis, a group of evolutionarily conserved ZMM proteins plays essential roles in stabilizing the recombination intermediates and promoting crossover (CO) formation. In mice, SHOC1 forms a trimeric complex with the other two ZMM proteins, SPO16 and TEX11, to bind recombination intermediates after strand invasion. Although genetic variants of SHOC1 are clinically associated with meiotic arrest and male infertility, their precise molecular mechanisms and evolutionarily conserved functions in human gametogenesis remain enigmatic. Here, we delineated species-specific divergences between human and mouse SHOC1 complex, and identified a missense variant within the XPF-like domain in SHOC1 (c.A1769G:p.Q590R) that was associated with meiotic arrest and non-obstructive azoospermia (NOA). The disorder of the XPF-like domain in SHOC1 impaired DNA double-strand breaks repair by compromising its ability to bind branched DNA structures and the recruitment of M1AP, REDIC1, and ZMM factors to recombination intermediates, ultimately abolishing CO formation. Furthermore, the variant disrupted dynamic 3D chromatin structure in pachytene spermatocytes and induced defects in homologous chromosome synapsis. More importantly, the XPF-like domain in SHOC1 was revealed to prevent autosome intrusion into the sex body compartment, thereby safeguarding critical autosomal loci from meiotic silencing of unsynapsed chromatin (MSUC). Overall, our study demonstrated that the XPF-like domain in SHOC1 is required for homologous recombination and safeguarding autosome from MSUC in meiosis.

developmental biology↗

bioRxiv2025

Testicular mRNA-LNP Delivery: A Novel Therapy for Genetic Spermatogenic Disorders

Uniform testicular maturation arrest is a severe form of male infertility characterized by the presence of germ cells that do not complete spermatogenic development. It is usually caused by meiotic arrest with genetic variants and difficult to treat via drugs or surgery. mRNA-lipid nanoparticle (LNP) delivery is a promising therapeutic option for maturation arrest with monogenic variants via protein replacement therapy. Herein, a spermatocytes-tropic LNP (Pool1-LNP3) was identified via a library of 30 ionizable lipids screening. And in vivo delivery of this novel LNP composition using rete testis microinjection was showed to be high spermatocytes targeting with high transfection efficiency. Thereafter, it was revealed that in vivo delivery of Pool1-LNP3 encapsulating Msh5 mRNA could promote crossover formation and restore spermatogenesis in Msh5D486Y/D486Y mouse models with DSB recombination defects. Notably, the offspring without genomic integration was born using intracytoplasmic sperm injection (ICSI) derived from rescue of Msh5D486Y/D486Ymouse and embryo transfer. Furthermore, no obvious inflammation and histologic damage in any tissue were detected after in vivo delivery of mRNA-LNP. In addition, it was demonstrated that Maps mRNA-LNP3 recovered spermatogenesis in Maps KO mouse with meiotic arrest. Altogether, these findings suggested that this spermatocytes-tropic mRNA-LNP delivery could become a viable and broad applicable strategy for treatment of spermatogenic disorders with genetic defects, providing a foundation for future clinical application.

molecular biology↗

bioRxiv2025

SPLiCR-seq: A CRISPR-Based Screening Platform for RNA splicing Identifies Novel Regulators of IRE1-XBP1 Signaling Under ER Stress

RNA splicing is fundamental to cellular function, yet systematic investigation of its complex regulation has been limited by existing methods. Here, we present SPLiCR-seq (SPLicing regulator identification through CRISPR screening), a high-throughput CRISPR screening platform that enables direct measurement of RNA splicing outcomes for pooled genetic perturbations, overcoming limitations of traditional fluorescence-based approaches. Applying SPLiCR-seq to investigate XBP1 splicing during the unfolded protein response (UPR), we conducted targeted and genome-wide screens across diverse cellular contexts, revealing both common and cell-type specific regulators. Notably, we identified GADD34 (PPP1R15A) as a novel modulator of IRE1-XBP1 signaling, demonstrating that it directly interacts with IRE1 and functions independently of its canonical role in eIF2 dephosphorylation. Pharmacological inhibition of GADD34 using Sephin1 effectively suppressed XBP1 splicing and alleviated CAR-T cell exhaustion in an ex vivo model, leading to enhanced tumor-killing capacity across multiple cancer models. This work not only establishes a powerful new tool for systematically studying RNA splicing regulation but also uncovers a promising therapeutic strategy for improving CAR-T cell immunotherapy through modulation of the IRE1-XBP1 pathway.

genetics↗