bims-scepro Biomed News
on Stem cell proteostasis
Issue of 2026–11–01
23 papers selected by
William Grey, University of York



  1. Cell Stem Cell. 2026 Oct 28. pii: S1934-5909(26)00380-2. [Epub ahead of print]
      Cell surface expression of the Slam family member CD150 is widely used for the prospective isolation of multipotent long-term hematopoietic stem cells (LT-HSCs). Here, we identify a bona fide endothelial protein C receptor (EPCR)+CD150- HSC subset, termed LT-HSC2, that sustains serial multi-lineage reconstitution. Long-term label-retaining assays reveal that LT-HSC2s are more deeply dormant than conventional EPCR+CD150+ LT-HSC1s, exhibit reduced cell cycle activation in response to inflammatory stress, and preserve stemness for prolonged periods in vivo. Moreover, combining EPCR with established HSC and multipotent progenitor (MPP) markers resolves the earliest stages of lineage divergence toward megakaryocytic/erythroid-biased CD150+ and lymphoid-biased CD150- trajectories. Thus, EPCR expression in HSCs and MPPs is associated with increased stemness, whereas CD150 expression does not encompass the full spectrum of long-term repopulating HSCs. Our findings establish EPCR+CD150- LT-HSC2s as a distinct, exceptionally dormant stem-cell subset and reveal an additional layer of HSC heterogeneity governing self-renewal, decreased stress sensitvity. and earliest lineage priming.
    Keywords:  CD150; LT-HSC; SLAM marker; dormancy; endothelial protein C receptor; epigenetic priming; hematopoietic stem cell; lineage differentiation; multipotent progenitor 6; self-renewal
    DOI:  https://doi.org/10.1016/j.stem.2026.09.016
  2. Cell Rep. 2026 Oct 29. pii: S2211-1247(26)01305-7. [Epub ahead of print]45(11): 118226
      Proteins shuttle between the nucleus and cytoplasm through the nuclear pore and via nuclear transport receptors, termed importins and exportins. Although genetic alterations involving nucleoporins are enriched in pediatric, adolescent, and young adult (AYA) acute myeloid leukemia (AML), nucleocytoplasmic transport has not been extensively studied in this disease. We discover that genes encoding nucleocytoplasmic transport pathway components (Kyoto Encyclopedia of Genes and Genomes [KEGG]: hsa03013) are enriched in AML cells from younger patients (≤40 years). Within this pathway, CSE1L is the highest expressed exportin in pediatric/AYA AML and shows minimal expression in hematopoietic stem cells (HSCs). CSE1L depletion reduces leukemic cell growth, proliferation, and clonogenic capacity, targeting leukemia stem cells while sparing normal HSCs. Mechanistically, we identify a novel Ran-GTP-dependent role for CSE1L in regulating pre-60S ribosomal subunit export in AML. Collectively, these data identify nucleocytoplasmic transport and ribosomal subunit export as enriched dependencies in pediatric/AYA AML and establish CSE1L-mediated export as a leukemic vulnerability.
    Keywords:  CP: cancer; CSE1L; XPO2; acute myeloid leukemia; childhood AML; nuclear export; nucleocytoplasmic transport; pediatric AML; ribosomal subunit export; ribosome biogenesis
    DOI:  https://doi.org/10.1016/j.celrep.2026.118226
  3. bioRxiv. 2026 Oct 07. pii: 2026.10.06.757119. [Epub ahead of print]
      Achieving near-single-cell precision in the prospective identification of long-term engrafting hematopoietic stem cells (LT-HSCs) remains challenging, likely because current static, point-in-time single-cell phenotyping technologies do not capture the dynamic nature of cell fate decisions. Here, we overcome this barrier by longitudinally tracking individual hematopoietic stem and progenitor cells (HSPCs) in ex vivo niche cultures using live imaging, coupled with downstream immunophenotyping, single-cell transcriptomics, and transplant assays. Deep learning analysis of live imaging data achieved 98.5% average precision in predicting serially-engrafting LT-HSC (serial-LT-HSC) identity from each cell's behaviorome (the totality of observed behaviors), outperforming currently available technologies. Serial-LT-HSCs exhibited lower motility among HSPC populations, which was associated with reduced Activin signaling activity and elevated expression of cell adhesion genes. Correspondingly, antagonizing Activin signaling by Inhibin-A treatment in ex vivo niche cultures suppressed HSPC motility while increasing the frequency of post-expansion serial-LT-HSCs, revealing a novel role for Activin signaling in HSPC behavior and fate determination. Collectively, this study establishes a broadly applicable framework that connects behavioromic analysis and single-cell transcriptomics to enable near-single-cell precision in predicting stem cell fate and uncover molecular mechanisms governing behavior-fate relationships.
    DOI:  https://doi.org/10.64898/2026.10.06.757119
  4. bioRxiv. 2026 Sep 02. pii: 2026.09.01.747091. [Epub ahead of print]
      Aged hematopoietic stem cells (HSCs) exhibit a shift from balanced to myeloid-biased differentiation, resulting in reduced lymphoid output and impaired adaptive immunity. The question of whether this lineage bias is established in a subset of HSCs during early development or primarily emerges with aging warrants further investigation. Here, we investigate whether myeloid-biased HSCs (my-HSCs) are established at the fetal liver stage by specifically examining Neogenin-1 (NEO1), a previously defined marker of my-HSCs. We identify two distinct populations of Hoxb5 + HSCs in the fetal liver: NEO1 + and NEO1, with NEO1 + HSCs exhibiting transcriptional and functional characteristics consistent with my- HSCs. With age, my-HSC-associated transcriptional programs become increasingly reinforced across the Hoxb5 + pHSC compartment, with NEO1 + cells showing early enrichment of this program and both NEO1 + and NEO1 - cells acquiring broader myeloid-biased features in aging. These findings suggest that lineage programming can begin early in development and is further shaped by age-related changes, potentially contributing to the functional decline observed in the aging hematopoietic system.
    DOI:  https://doi.org/10.64898/2026.09.01.747091
  5. Nat Immunol. 2026 Nov;27(11): 2306-2321
      Embryonic hematopoiesis is thought to occur exclusively in the extraembryonic yolk sac before hematopoietic stem cells (HSCs) arise in the aorta-gonad-mesonephros region. Here we identify a previously unrecognized hematopoietic site at the maternal-fetal interface in mice, termed MIXER (Maternally Interfaced eXtraEmbRyonic) tissue, which develops contemporaneously with the yolk sac and exhibits robust hematopoietic activity. MIXER contains abundant hematopoietic precursors, including classical CSF1R+ erythro-myeloid progenitors and a unique embryonic CD4+CSF1R- Erythro-Myeloid PRogenitOR (eEMPROR) population. Lineage-tracing experiments demonstrate that eEMPROR cells contribute to select macrophage subpopulations during fetal development, primarily in the perivascular space. Notably, early human placental villi, before HSC emergence, also harbor CD4+ nucleated erythrocytes, indicating a conserved hematopoietic role for the maternal-fetal interface. These findings establish MIXER as an anatomically distinct niche for embryonic hematopoiesis and expand the developmental map of blood cell emergence in mammals.
    DOI:  https://doi.org/10.1038/s41590-026-02683-4
  6. Leukemia. 2026 Oct 28.
      The hyperactive kinase FLT3-ITD causes acute myeloid leukemia (AML) and is a prognostic biomarker. We synthesized and characterized MA191 as a novel von Hippel-Lindau (VHL) E3 ubiquitin ligase-based proteolysis targeting chimera (PROTAC) for FLT3. MA191 induces apoptosis in cultured and primary AML patient cells harboring FLT3-ITD (IC50=9.6-11 nM; EC50=0.001-0.883 µM). Comparison with a VHL-binding-deficient stereoisomer of MA191 demonstrates that FLT3-ITD degradation is superior to kinase inhibition (p < 0.03). Rapid depletion of FLT3-ITD by MA191 (DC50=10 nM) requires VHL, neddylation, proteasome activity, and the pro-apoptotic BH3-only protein BIM. MA191 reduces FLT3-ITD prior to apoptosis, uncovering apoptosis-independent roles of BIM for protein stability. Higher expression levels of FLT3 in leukemia cells than in healthy cells (n = 3675/n = 1249) are associated with worse AML patient survival (p = 0.0099). MA191 does not harm healthy blood and bone marrow progenitor cells or myeloid cell differentiation. In Danio rerio larvae, MA191 halts AML cell proliferation without significant toxicity. Human stromal cell interactions and mutations in the tyrosine kinase domain of FLT3-ITD that confer resistance to FLT3 inhibitors do not abolish anti-leukemic effects of MA191. Accordingly, leukemia cells with acquired resistance to MA191 lack such mutations. We offer a framework for fast-acting next-generation FLT3 degraders that overcome resistance mechanisms to classical inhibitors.
    DOI:  https://doi.org/10.1038/s41375-026-03168-x
  7. Autophagy. 2026 Oct 29. 1-33
      Modification by ubiquitination governs the half-lives of thousands of proteins that are fated for elimination by either the proteasome or autophagy pathways, depending on the intricate architectures of ubiquitin modification. This system mediates quality control for individual proteins, protein complexes, and organelles, as well as myriad purely regulatory functions. Here we provide a comprehensive survey of the ubiquitin-proteasome system (UPS), the scope of which is at present poorly defined. The UPS, with the inclusion of pathways involving ubiquitin-like modifiers, comprises in our estimate over 1430 distinct components in humans, a vast set of activities whose collective impact on the biology of the cell is pervasive. The UPS is an integral component of the proteostasis network (PN), the remainder of which is surveyed in the accompanying reports. With the addition of molecular chaperones, proteins from autophagy-lysosome pathway, and related activities, the PN includes in total over 3150 components by our estimates. Comprehensive and systematic definition of these pathways should facilitate a range of ongoing investigations in the areas of genomics, proteomics, biochemistry, cell biology, and disease research.Abbreviations: APC, anaphase promoting complex; CDD, Conserved Domain Database; CRL, cullin RING ligase; DSB, double-strand break; DUB, deubiquitinating enzyme; ERAD, ER-associated degradation; PN, proteostasis network; RBR, RING-between-RING; RCR, RING-Cys-Relay; SPOC, Structure Prediction and Omics-informed Classifier; UB, ubiquitin; UBL, ubiquitin-like; UBLM, ubiquitin-like modifier; UEV, ubiquitin-conjugating enzyme variant; UPS, ubiquitin-proteasome system.
    Keywords:  Cullin; UFMylation; deubiquitination; sumoylation; ubiquitin ligase; ubiquitin-like modifier
    DOI:  https://doi.org/10.1080/15548627.2026.2741092
  8. Autophagy. 2026 Oct 28. 1-14
      The condition of having a healthy, functional proteome is known as protein homeostasis, or proteostasis. Establishing and maintaining proteostasis is the province of the proteostasis network, a highly interconnected system of over 3000 components that regulate protein synthesis, folding, localization, and degradation. The proteostasis network is a fundamental functional unit in biology that is essential for cellular health and has direct relevance to many diseases of protein conformation. However, it is not well defined or annotated, hindering its functional characterization in health and disease. In this series of manuscripts, we aim to operationally define the human proteostasis network by providing a comprehensive, annotated list of its components. In the other manuscripts in this series, we survey the components of the proteostasis network that make up (1) the machineries for protein synthesis, protein folding, protein trafficking into and out of organelles, and organelle-specific degradation pathways and (2) the ubiquitin-proteasome system. Here, we have compiled a curated list of over 850 unique high-confidence components of the autophagy-lysosome pathway, the other major protein degradation system in human cells. This resource will facilitate the rigorous investigation of autophagy-lysosome pathway dysfunction as a driver of proteostasis imbalance in aging and disease.
    Keywords:  Aging; annotation; degradation; lysosomal catabolism; neurodegenerative disease; systems
    DOI:  https://doi.org/10.1080/15548627.2026.2741038
  9. Front Cell Dev Biol. 2026 ;14 1980188
      Acute myeloid leukemia (AML) is a genetically heterogeneous hematological malignancy in which chemoresistance and relapse, often driven by leukemia stem cells (LSCs), remain major obstacles to cure. Autophagy is an evolutionarily conserved lysosomal degradation pathway whose function in AML is not fixed but is stage- and context-dependent: it restrains leukemogenesis in some settings while sustaining established and therapy-stressed LSCs in others. The Bcl-2-associated athanogene 3 (BAG3)-heat shock protein 70 (HSP70) axis integrates proteotoxic stress with the autophagy machinery, most notably through chaperone-assisted selective autophagy (CASA). This review applies a four-tier evidence framework-direct AML evidence, other hematological evidence, non-AML evidence, and proposed or hypothetical mechanisms-and explicitly separates BAG3-specific evidence from general HSP70 and autophagy findings. Direct AML evidence is comparatively strong for the cytoprotective, mitophagic and chemoresistance roles of autophagy and HSP70, but it is limited for a specific BAG3 dependency. In particular, direct BAG3 coupling to ULK1, competitive BAG3/HSP70 binding at the Beclin1 BH3 domain, and direct HSP70 shielding of ATG5 from cleavage are not supported by primary evidence. We examine the crosstalk between this axis and recurrent AML alterations (FLT3-ITD, NPM1 and TP53), and survey therapeutic strategies ranging from ATP-site HSP70 inhibitors to HSP70-BAG3 protein-protein interaction inhibitors, dual HSP70/HSP90 targeting, BAG3-directed agents, targeted protein degradation, nanoparticle delivery and emerging immunotherapies. We stratify direct axis-targeting from broad HSP70-family or proteostasis approaches. Finally, we summarize the principal knowledge gaps and the potential therapeutic window, cardiac-safety and biomarker challenges that must be addressed to convert the BAG3-HSP70 axis from a plausible mechanism into a precision target in AML.
    Keywords:  BAG3; HSP70; acute myeloid leukemia; autophagy; chaperone-assisted selective autophagy; chemoresistance; leukemia stem cells; targeted therapy
    DOI:  https://doi.org/10.3389/fcell.2026.1980188
  10. NPJ Precis Oncol. 2026 Oct 29. pii: 412. [Epub ahead of print]10(1):
      Acute myeloid leukemia (AML) with IDH1 mutations is amenable to targeted therapy, highlighting the need for reliable identification. We developed an attention-based multiple-instance learning model to predict IDH1 mutation status using bone marrow smear whole-slide images from 436 AML patients across four centers in Germany and the US, achieving a mean single pooled ROC-AUC of 0.81. In top tile analysis, model predictions for IDH1 were associated with immature leukemia phenotypes.
    DOI:  https://doi.org/10.1038/s41698-026-01762-x
  11. Autophagy. 2026 Oct 27. 1-15
      The condition of having a healthy, functional proteome is known as protein homeostasis, or proteostasis. Maintaining proteostasis is the province of the proteostasis network, which consists of the cellular components that regulate protein synthesis, folding, localization, and degradation. The proteostasis network is a fundamental functional unit in biology with relevance to many diseases. Despite its importance, the human proteostasis network has until now lacked a precise definition, limiting our ability to interrogate proteostasis, integrate multiomic datasets, compare results across studies, or model proteostasis dysfunction in disease. To address this limitation, we have operationally defined the human proteostasis network by providing a comprehensive, annotated, and manually curated list of its components classified into nine Branches based on their function and localization - cytonuclear proteostasis, ER proteostasis, mitochondrial proteostasis, nuclear proteostasis, proteostasis network regulation, translation, extracellular proteostasis, the autophagy-lysosome pathway, and the ubiquitin-proteasome system - which we present in a series of three manuscripts of which this is the first. Overall, the proteostasis network annotation encompasses 3,151 components described by 4,043 annotations. Here, we present the 1,190 components that make up the first seven of these Branches, which comprise the compartment-based proteostasis network (cytonuclear, ER, mitochondrial, nuclear, and extracellular proteostasis), proteostasis network regulation, and translation. These Branches include chaperones, folding enzymes, systems for trafficking proteins, organelle-specific degradation systems, and the cell's translation machinery. This work provides a framework that will facilitate insights into how proteostasis is preserved in health, lost in aging and disease, and how it could be restored through pharmacological intervention.
    Keywords:  Annotation; cellular stress responses; chaperones; protein folding; protein synthesis; protein transport
    DOI:  https://doi.org/10.1080/15548627.2026.2741033
  12. bioRxiv. 2026 Aug 31. pii: 2025.05.22.655512. [Epub ahead of print]
      Parallelization of data acquisition substantially increases the throughput of mass spectrometry-based proteomics. However, parallelization also increases the density of mass spectra and consequently the overlap between ions, frustrating their analysis. To improve sequence identification and quantification from such spectra, we developed an open-source software for Joint Modeling of mass spectra (JMod). JMod models overlapping peaks as linear super-positions of their components in both MS1 and MS2 space, which permits multiplexed DIA with smaller mass offsets to increase the multiplexing capacity and thus proteomics through-put for a given plexDIA tag. This enables 9-plexDIA using 2 Da offset PSMtags, increasing throughput 9-fold while preserving quantitative accuracy and coverage depth. Furthermore, we use JMod to deconvolve simultaneous labeling by mass tags and heavy amino acids, thus increasing the throughput of metabolic pulse experiments measuring protein synthesis and degradation rates in single cells from mouse liver. By supporting enhanced decoding of highly multiplexed DIA spectra, JMod provides an open and flexible software that increases the throughput of sensitive proteomics.
    DOI:  https://doi.org/10.1101/2025.05.22.655512
  13. Autophagy. 2026 Oct 26. 1-28
      The retinal pigment epithelium (RPE) sustains lifelong proteostasis under chronic stress, yet how post-mitotic cells activate macroautophagy/autophagy when canonical kinase pathways suppress it remains unresolved. Here we demonstrate that AKT1 (protein kinase B alpha), drives autophagy through a non-canonical transcriptional mechanism triggered by isoform imbalance. In RPE and age-related macular degeneration (AMD) models, AKT2 (protein kinase B beta) hyperactivation destabilizes MTORC2 (mechanistic target of rapamycin complex 2) and engages RPS6KB/S6K (ribosomal protein S6 kinase beta) -mediated IRS-1 (insulin Receptor Substrate 1) inhibition, creating a feedforward autophagic arrest. Compensatory AKT1 activation via MTORC2 phosphorylates TERT (telomerase reverse transcriptase) at serine 824, driving nuclear translocation that is independent of telomere maintenance. In the nucleus, TERT assembles with FOXO3 (forkhead Box O3) and MYC (MYC proto-oncogene, bHLH transcription factor) into a tripartite transcriptional complex that occupies the EIF2AK3/PERK promoter (eukaryotic translation initiation factor 2-alpha kinase 3/ protein kinase R-like endoplasmic reticulum kinase), enabling EIF2AK3 transcriptional activation. This activity converts the unfolded protein response from pro-apoptotic to cytoprotective: EIF2AK3-ATF4 (activating transcription factor 4) signaling promotes core autophagy machinery biogenesis and selective ERphagy through the receptors TEX264 (testis expressed 264) and CCPG1(cell cycle progression 1), which prevents pathological EIF2AK3 clustering and preserves tubular ER architecture in diseased RPE. Using C. elegans phosphorylation-deficient mutants, mouse models and AMD patient iPSC-RPE, we establish that AKT1-mediated TERT phosphorylation is an evolutionarily conserved prerequisite for FOXO/DAF-16 nuclear function and lysosomal homeostasis in post-mitotic cells, offering therapeutic potential through targeted pharmacologic inhibition of AKT2.Abbreviations: ACTB: actin, beta; AKT1: AKT serine/threonine kinase 1; AKT2: AKT serine/threonine kinase 2; ALP: autophagy-lysosomal pathway; AMD: age-related macular degeneration, ATF4: activating transcription factor 4; ATG3: autophagy related 3; ATG4B: autophagy related 4B cysteine peptidase; ATG7: autophagy related 7; CCPG1: cell cycle progression 1; CFH: complement factor H; C57BL/6J: C57 black 6J; DMSO: dimethyl sulfoxide; MYC: MYC proto-oncogene, bHLH transcription factor; EIF2A/eIF2α: eukaryotic translation initiation factor 2A; EIF2AK3/PERK: eukaryotic translation initiation factor 2 alpha kinase 3; ER: endoplasmic reticulum; ERN1/IRE-1α: endoplasmic reticulum to nucleus signaling 1; ERphagy: endoplasmic reticulum-selective autophagy; FOXO1: forkhead box O1; FOXO3: forkhead box O3; iPSC-RPE: induced pluripotent stem cell-derived retinal pigment epithelium; ITGB1/integrin β1: integrin subunit beta 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAPKAP1/SIN1: MAPK associated protein 1; MTOR: mechanistic target of rapamycin kinase; MTORC1: MTOR complex 1; MTORC2: MTOR complex 2; PBS: phosphate-buffered saline; PI3K: phosphoinositide 3-kinase; RICTOR: RPTOR independent companion of MTOR complex 2; RPE: retinal pigment epithelium; RPTOR: regulatory associated protein of MTOR complex 1; SQSTM1/p62: sequestosome 1; TERT: telomerase reverse transcriptase; TEX264: testis expressed 264, ER-phagy receptor; UPR: unfolded protein response; VCL: vinculin; WT: wild type.
    Keywords:  AKT1; Age-Related Macular Degeneration (AMD); EIF2AK3/PERK-ATF4 signaling; Telomerase Reverse Transcriptase (TERT); autophagy/Erphagy; proteostasis
    DOI:  https://doi.org/10.1080/15548627.2026.2750048
  14. Nature. 2026 Oct 28.
      The N7-methylguanosine (m7G) modification is one of the most prevalent tRNA modifications, mainly catalysed by the METTL1-WDR4 protein complex1-4. The m7G methyltransferase METTL1 has been linked to oncogenic transformation and the maintenance of several aggressive malignancies; however, the clinical implications of therapeutically targeting a tRNA-modifying enzyme have not been established. Here we present the development and characterization of STM9005, a highly selective and potent first-in-class tRNA methyltransferase inhibitor of METTL1. Treatment of numerous cancer cell models (including leukaemia, melanoma, pancreatic carcinoma, oesophageal cancer and small cell lung carcinoma) with STM9005 blocks cell growth, causes differentiation changes and dysregulates cell cycle progression. These cellular effects were accompanied by a selective decrease in m7G on a subset of tRNAs and a reduction in their expression levels, which impacted the translation of oncogenic mRNAs. We show that pharmacological inhibition of METTL1 in vivo impairs tumour growth and significantly prolongs survival in multiple mouse cancer models of different tissue origin. Collectively, our results provide a strong proof of concept that targeting of tRNA methylation is a promising avenue of anti-cancer therapy and illustrate that catalytic inhibition of METTL1 represents a therapeutic strategy against a number of aggressive malignancies.
    DOI:  https://doi.org/10.1038/s41586-026-11178-z
  15. Adv Sci (Weinh). 2026 Oct 28. pii: e78403. [Epub ahead of print]
      Resistance to bortezomib (BTZ) represents a major obstacle that limits the therapeutic efficacy and worsens the prognosis of multiple myeloma (MM). Ferroptosis, a form of regulated cell death triggered by excessive lipid peroxidation, has garnered increasing attention for anticancer intervention, yet the mechanisms underlying ferroptosis in MM remain enigmatic. Here, we confirmed that ALDH2 is upregulated in MM patients and that its altered expression is closely associated with BTZ resistance and poor prognosis. Functionally, ALDH2 promoted the proliferation, BTZ resistance, and ferroptosis resistance of MM cells, suggesting its oncogenic role. Mechanistically, ALDH2 competitively bound to KEAP1 and stabilized NRF2 by preventing its ubiquitin-proteasome-mediated degradation, thereby promoting the nuclear translocation of NRF2 and subsequent upregulation of GPX4, and in turn regulating ferroptosis, proliferation, and BTZ resistance in MM. In parallel, NRF2 bound directly to the promoter region of ALDH2 and further enhanced ALDH2 transcription, thus forming a positive feedback loop. Collectively, our findings reveal that the ALDH2/KEAP1/NRF2-GPX4 axis may serve as a key regulator of ferroptosis in MM and a promising therapeutic target for overcoming BTZ resistance.
    Keywords:  ALDH2; Multiple myeloma; bortezomib resistance; ferroptosis
    DOI:  https://doi.org/10.1002/advs.78403
  16. Cell Death Dis. 2026 Aug 01. pii: 919. [Epub ahead of print]17(1):
      Inflammasomes are innate immune signaling platforms that activate caspase-1, which in turn cleaves gasdermin D (GSDMD) into its mature form, leading to pyroptosis, an inflammatory form of regulated necrosis. It has been reported that bacterial lipopeptides (BLPs) trigger pyroptosis through NLRP7 inflammasome activation. However, the underlying recognition mechanism remains entirely unclear, and the concept of BLP sensing by NLRP7 has not been well established. In this study, we sought to elucidate the mechanism by which BLPs induce inflammasome activation and pyroptosis in human acute myeloid leukemia cell lines. Through comprehensive analyses, we demonstrate that BLPs induce GSDMD-dependent pyroptosis not via the NLRP7 inflammasome, but through the NLRP3 inflammasome without the need for additional stimuli. Addition of KCl to the culture medium significantly suppressed BLP-induced pyroptosis, suggesting the involvement of K+ efflux in inflammasome activation. However, BLPs alone are generally thought to be insufficient to directly induce K+ efflux, and K+ channel inhibitors had minimal effects, prompting us to hypothesize that K+ efflux might result from sublethal membrane damage associated with a distinct cell death mechanism. Among several cell death inhibitors tested, reducing agents, inhibitors of disulfidptosis, which is necrotic cell death caused by excessive disulfide bonding in the actin cytoskeleton, markedly attenuated BLP-induced K+ efflux and pyroptosis. Consistent with this, BLP stimulation led to NADPH depletion and increased disulfide bond formation in β-actin, hallmarks of disulfidptosis. These findings suggest that disulfide stress contributes to NLRP3 inflammasome activation and pyroptosis triggered by BLPs in leukemia cells. To our knowledge, this is the first report linking disulfidptosis-associated disulfide stress to innate immune signaling, providing a conceptual framework for exploiting pyroptosis induction in leukemia cells.
    DOI:  https://doi.org/10.1038/s41419-026-09164-4
  17. bioRxiv. 2026 Oct 10. pii: 2026.10.01.755757. [Epub ahead of print]
      The mammalian BRG-/BRM-associated factor (BAF) chromatin remodeling complexes are crucial regulators of hematopoietic stem and progenitor cell (HSPC) fate. Expression of the ncBAF subcomponent, BRD9, is altered in both normal aging and myeloid malignancies. We find that in adult human HSPC, BRD9 regulates the differentiation of myeloid progenitors. Upon degradation of BRD9 in these cells, ncBAF is displaced from the chromatin, leading in turn to enhanced recruitment of cBAF to bona fide CEBPA target sites. With the shift from ncBAF to cBAF, HSPC differentiation results in increased generation of myeloid-derived suppressor cells (MDSC) that secrete elevated levels of IL-8. Soluble factors from these myeloid cells, which have lost BRD9, enhance the stemness of breast cancer cells in vitro. In contrast, bromodomain inhibition of BRD9 results in minimal alterations of ncBAF binding and myeloid differentiation, indicating that BRD9 acts as a barrier to human MDSC differentiation in a bromodomain-independent manner.
    KEY POINTS: BRD9 suppresses the development of myeloid-derived suppressor cells in a bromodomain-independent mannerLoss of BRD9 results in increased cBAF recruitment to CEBPA target sites and enhanced myeloid differentiation.
    DOI:  https://doi.org/10.64898/2026.10.01.755757
  18. bioRxiv. 2026 Oct 08. pii: 2026.10.01.756000. [Epub ahead of print]
      CBFA2T3-GLIS2 (C/G) defines a high-risk pediatric AML subtype in which de novo enhancer rewiring sustains an aggressive leukemic transcriptional state. The early epigenomic mechanisms reinforcing this program and linking it to leukemic survival remain incompletely defined. Here, we identify enhancer-proximal hypermethylation as a noncanonical, transcription-permissive feature of C/G AML. Using primary C/G-positive AML samples and a developmentally relevant C/G-transformed cord blood hematopoietic stem/progenitor cell model, we integrated DNA methylation, chromatin state, fusion occupancy, and gene expression across early and leukemia-stage contexts. Early C/G-associated hypermethylated regions localized near H3K27ac/H3K4me1-marked active or primed cis-regulatory elements, were enriched for ERG/ETS-like motifs, and showed related architecture in leukemia-stage contexts. DNMT3B was prominently increased in C/G contexts, and its loss selectively altered methylation-associated gene expression without measurably changing global 5mC. Genetic DNMT3B loss increased venetoclax sensitivity in vitro, while pharmacologic DNMT3B inhibition with Nanaomycin-A similarly enhanced venetoclax response. During venetoclax treatment, DNMT3B-deficient xenografts showed reduced disease burden and prolonged survival. To assess whether this interaction extended to clinically used hypomethylating agents, azacitidine or decitabine plus venetoclax induced apoptosis-related transcriptional programs and mitochondrial depolarization. These findings identify hypermethylated active cis-regulatory elements as C/G-associated states linked to transcriptional dysregulation and venetoclax response.
    DOI:  https://doi.org/10.64898/2026.10.01.756000
  19. Nat Cell Biol. 2026 Oct 29.
      Although mRNA decoding efficiency influences protein synthesis, it remains unknown whether the translation elongation machinery harbours intrinsic mechanisms that selectively modulate codon decoding to shape proteomes. Here we show that METTL13-catalysed dimethylation of the elongation factor eEF1A at lysine 55 (eEF1AK55me2) enhances decoding of select codons, preferentially increasing pro-oncogenic protein synthesis to promote tumorigenesis and targeted therapy resistance. Proteomic profiling and single-molecule imaging reveal that eEF1AK55me2 increases decoding efficiency, particularly for under-represented codons with weak wobble-position base pairing. In cancer cells, METTL13 knockdown reduced translation of oncogenic mRNA enriched in eEF1AK55me2-dependent codons, including KRAS; synonymous recoding with eEF1AK55me2-independent codons reversed this effect. METTL13 loss inhibited the growth of KRASG12C inhibitor (sotorasib)-resistant lung adenocarcinoma syngeneic tumours and patient-derived xenografts. In relapsed autochthonous KRASG12C-driven lung adenocarcinoma, METTL13 ablation mitigated sotorasib resistance and significantly extended survival in vivo. Among patients receiving a KRASG12C inhibitor, inferred METTL13 activity was associated with inferior clinical response. These findings identify an eEF1AK55me2-mediated mRNA decoding mechanism promoting selective oncogenic protein synthesis and suggest METTL13 targeting may counteract KRAS-inhibitor resistance.
    DOI:  https://doi.org/10.1038/s41556-026-02085-6
  20. bioRxiv. 2026 Sep 04. pii: 2026.09.01.748392. [Epub ahead of print]
      Obesity expands myeloid progenitors, myelopoiesis and increases the production of monocytes. While weight loss (WL) alleviates aspects of this inflammatory dysregulation, it is not known whether GLP-1 receptor agonists or other traditional modalities of WL differentially modify hematopoietic stem/progenitor cells (HSPCs), hematopoiesis, or inflammatory cell production. To test this, we compared the hematopoietic compartment in lean, obese and weight-reduced mice from tirzepatide treatment and caloric restriction (CR) implemented to match the body weight in both groups. At equal WL, we found CR induced multilineage cytopenias, whereas tirzepatide preserved blood lineages while specifically reducing classical Ly6Chi CCR2+ monocytes. To define the mechanisms underlying these changes we performed single-cell mRNA sequencing of bone marrow HSPCs and mature mononuclear blood cells. CR-HSPCs suppressed gene sets associated with nutrient sensing, proliferation and oxidative phosphorylation (OXPHOS) and exhibited lower inferred cell cycle activity, whereas tirzepatide-HSPCs attenuated these changes. Unlike CR, we found that across progressively differentiated cells from HSPCs to mature blood monocytes, tirzepatide increasingly suppressed OXPHOS and simultaneously shifted the maturation spectrum away from classical monocytes. Following six weeks of tirzepatide withdrawal and weight regain, Ly6Chi CCR2+ monocytes rebounded to levels seen in obese mice. These findings suggest that tirzepatide uncouples WL from the broad hematopoietic suppression seen in CR by preserving progenitor activity but selectively remodeling inflammatory/classical monocytes. We demonstrate that WL modality differentially impacts hematopoietic adaptation and provide evidence that classical monocytes are an effector cell through which tirzepatide may dampen obesity-associated inflammation.
    DOI:  https://doi.org/10.64898/2026.09.01.748392
  21. bioRxiv. 2026 Oct 07. pii: 2026.09.30.755742. [Epub ahead of print]
      Cell-cell communication underpins intercellular responses allowing cells to dynamically change states across conditions; however current methods typically aggregate signals by cell type annotations which may introduce biases. We developed HyperCom, a hypergraph-based method to infer cell-resolved cell-cell communication from single cell transcriptomics data. HyperCom constructs a hypergraph from known ligand-receptor interactions and the expression of those ligands and receptors in individual cells and performs graph diffusion on the hypergraph to score cells on a continuous spectrum from sender to receiver for each LR pair. HyperCom then generates a cell-type agnostic ranking of LR pairs by communication either over the whole dataset or in a condition-aware manner. Validation of HyperCom on physical cell-to-cell contact, spatial, and multicondition datasets highlight its flexibility to capture subtle per cell communication information. HyperCom is available as a species-agnostic, scalable, and open source R package: https://github.com/pawelab/HyperCom.
    DOI:  https://doi.org/10.64898/2026.09.30.755742
  22. Nat Struct Mol Biol. 2026 Oct 28.
      The cell surface proteome governs processes essential for development, immunity and disease, yet its large-scale spatial organization remains uncharted. Here, we systematically map the surface proteome of human T lymphocytes and B lymphoblasts using proximity labeling of 85 antigens. Coupled with data-independent acquisition mass spectrometry, this approach reveals functional modules, including known complexes such as the T cell receptor alongside clusters not previously implicated in cell membrane functions. Notably, we identify mitochondrial proteins at the surface, suggesting that they may bear underappreciated roles at the plasma membrane. A machine learning classifier predicts surface protein associations, revealing the IL-10 receptor beta subunit's regulation of type I interferon signaling. Spatial modeling distinguishes widely dispersed from localized antigens, indicating active mechanisms of surface organization. In summary, this work provides a large-scale map of the human surfaceome and a resource for exploring its spatial and functional organization.
    DOI:  https://doi.org/10.1038/s41594-026-01914-4
  23. Cell Death Discov. 2026 Jul 29. pii: 426. [Epub ahead of print]12(1):
      Small Heat Shock Protein Family B (HSPB) members are ATP-independent chaperones essential for maintaining cellular proteostasis. Together with chaperones and co-chaperones such as HSP70 and BAG3, they prevent aberrant protein folding and suppress protein aggregation, particularly under proteotoxic stress. HSPBs have also been extensively linked to neurodegenerative disease and in promoting chemoresistance in cancer. We previously showed that members of the HSPB family can reside within the mitochondrial intermembrane space where they contribute to the maintenance of proteostasis, and that acute cytotoxic stress leads to HSPB sequestration to the outer mitochondrial membrane. Here, we further elucidate this mechanism, demonstrating that HSPB1 is selectively enriched within mitochondria under milder thermal stress condition, exhibiting a pronounced association with the outer mitochondrial membrane. We also observed distinct stress-dependent mitochondrial recruitment profiles across HSPB paralogs, revealing a similar behaviour for HSPB8, whereby HSPB1 responded at a comparatively lower stress threshold, indicating functional specialization within the HSPB family. Inducing this mechanism enhances cell survival during hyperthermic stress, preventing Cytochrome c release, and raising the apoptotic activation threshold in our experimental system. These findings indicate that HSPBs, particularly HSPB1 may contribute to mitochondrial stress adaptation prior to Cytochrome c release. This underexplored mechanism may underlie the modulation of stress-related and degenerative disease progression and contribute to the chemoresistance associated with cancer, which have been attributed to HSPBs.
    DOI:  https://doi.org/10.1038/s41420-026-03268-8