Molecular Biology of the Cell最新文献_第2页

Local RhoA activation induces anillin-independent septin recruitment in interphase cells. 局部RhoA激活诱导间期细胞中抗青霉素非依赖性septin的募集。

IF 2.7 3区生物学

Molecular Biology of the Cell Pub Date : 2026-05-01 Epub Date: 2026-03-25 DOI: 10.1091/mbc.E25-09-0468

Shreya Chandrasekar, Margaret E Utgaard, Bradley Somerfield, Huini Wu, Jordan R Beach, Patrick W Oakes

{"title":"Local RhoA activation induces anillin-independent septin recruitment in interphase cells.","authors":"Shreya Chandrasekar, Margaret E Utgaard, Bradley Somerfield, Huini Wu, Jordan R Beach, Patrick W Oakes","doi":"10.1091/mbc.E25-09-0468","DOIUrl":"10.1091/mbc.E25-09-0468","url":null,"abstract":"The regulation of the actin cytoskeleton is key to controlling cell shape and structure. While the Rho GTPase RhoA is well known to regulate the actomyosin cytoskeleton, its function in controlling the septin cytoskeleton remains unclear. As RhoA interactions can vary in both time and space, they can be challenging to discern from traditional bulk biochemical assays. Here, we use multiple optogenetic tools to spatially and temporally increase myosin localization, stimulate contractile force, and activate RhoA to investigate how RhoA and its downstream effector myosin impact the septin cytoskeleton. We find that neither local accumulation of myosin nor increased activity of myosin is sufficient to alter septin architecture. Local activation of RhoA, however, results in a local increase in septin accumulation. Importantly, this septin increase is independent of the scaffolding protein anillin, which can directly bind both septin and RhoA. Together, these data expand the potential role of septins in mediating RhoA signaling by stimulating the remodeling of the septin cytoskeleton.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"ar42"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147513440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ATG9B regulates mitochondrial integrity and apoptotic tumor cell death. ATG9B调控线粒体完整性和肿瘤细胞凋亡

IF 2.7 3区生物学

Molecular Biology of the Cell Pub Date : 2026-05-01 Epub Date: 2026-03-11 DOI: 10.1091/mbc.E25-07-0334

Hong Cao, Lixia Guo, Jing Chen, Eugene Krueger, Gina Razidlo, Mark A McNiven

{"title":"ATG9B regulates mitochondrial integrity and apoptotic tumor cell death.","authors":"Hong Cao, Lixia Guo, Jing Chen, Eugene Krueger, Gina Razidlo, Mark A McNiven","doi":"10.1091/mbc.E25-07-0334","DOIUrl":"10.1091/mbc.E25-07-0334","url":null,"abstract":"It is well established that many tumor types possess defective autophagic pathways. Several studies have reported that the transmembrane, autophagic lipid scramblase ATG9B is altered in multiple cancers, suggesting that this dysregulation could contribute to oncogenesis. Therefore, the goal of this study was to define the cellular distribution of ATG9B in two different tumor cell types and to provide insights into its cellular function. Surprisingly, we found that ATG9B shows a modest association with autophagic structures and exhibits a unique and prominent localization to mitochondria, in contrast to its related form ATG9A. Upon expression of tagged ATG9B forms, this mitochondrial distribution was accompanied by aberrant changes in mitochondrial morphology as well as a reduction in the mitochondrial membrane potential and the release of mtDNA. Few indicators for ATG9B-dependent mitophagy were noted. Instead, ATG9B overexpression led to pronounced apoptotic cell death as assessed by a variety of indicators. Further, we find that the N-terminal sequence of ATG9B acts as a mitochondrial targeting domain and that expression of this peptide alone can induce apoptotic cell death. These findings provide new insights into a putative cellular localization and function for ATG9B.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"ar44"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147434291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The microtubule GTP-tubulin cap size is modulated during cell division. 微管gtp -微管蛋白帽大小在细胞分裂过程中被调节。

IF 2.7 3区生物学

Molecular Biology of the Cell Pub Date : 2026-05-01 Epub Date: 2026-03-11 DOI: 10.1091/mbc.E26-01-0054

Anna C Cassidy, Dylan T Burnette, Marija Zanic

{"title":"The microtubule GTP-tubulin cap size is modulated during cell division.","authors":"Anna C Cassidy, Dylan T Burnette, Marija Zanic","doi":"10.1091/mbc.E26-01-0054","DOIUrl":"10.1091/mbc.E26-01-0054","url":null,"abstract":"Microtubule dynamics change during cell division to enable rapid microtubule network remodeling. The switching from microtubule growth to shrinkage is attributed to the loss of a stabilizing GTP-cap structure at the growing microtubule end. The size of the GTP-cap is a result of a balance between GTP-tubulin addition to the microtubule end and subsequent GTP-hydrolysis in the microtubule lattice. Whether the cell-cycle-dependent changes in microtubule dynamics are supported by concurrent modulation of the stabilizing GTP-cap size is not known. Here, we use high spatiotemporal resolution live-cell imaging of EB1, an established marker for the GTP-cap, to directly determine the relationship between GTP-cap size and microtubule growth rate throughout the cell cycle. Our data reveal that GTP-cap size for matching growth rates is reduced during mitosis. Comparison of EB1 comets on astral versus spindle microtubules reveals that the scaling between the GTP-cap size and microtubule growth rate is not spatially regulated in mitosis. We find that these regulatory patterns are conserved across epithelial cells from two different species. Taken together, our findings reveal modulation of GTP-cap size as a cell-cycle-regulated mechanism for tuning microtubule stability.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"br14"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147434261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MCTP1 and MCTP2 promote ER-PM contact sites and regulate PI4P homeostasis and cell migration. MCTP1和MCTP2促进ER-PM接触位点，调节PI4P稳态和细胞迁移。

IF 2.7 3区生物学

Molecular Biology of the Cell Pub Date : 2026-05-01 Epub Date: 2026-03-25 DOI: 10.1091/mbc.E25-09-0445

Suganthan Amirthagunanathan, Maxime Boutry, Vasudeva Tati, Dibyayan Maity, Caroline Chapman, Madhura R Pandkar, Brian Raught, Peter K Kim, Amit S Joshi

引用次数: 0

RANKL-inducible Arl8b effector RUFY4 drives HOPS-mediated lysosomal maturation and trafficking in osteoclasts. rankl诱导的ar18b效应物RUFY4驱动hops介导的溶酶体成熟和破骨细胞运输。

IF 2.7 3区生物学

Molecular Biology of the Cell Pub Date : 2026-05-01 Epub Date: 2026-04-02 DOI: 10.1091/mbc.E25-08-0412

Kshitiz Walia, Gaurav Kumar, Subhash B Arya, Priya Chouhan, Arshdeep Kaur, Medha Gupta, Amit Tuli

{"title":"RANKL-inducible Arl8b effector RUFY4 drives HOPS-mediated lysosomal maturation and trafficking in osteoclasts.","authors":"Kshitiz Walia, Gaurav Kumar, Subhash B Arya, Priya Chouhan, Arshdeep Kaur, Medha Gupta, Amit Tuli","doi":"10.1091/mbc.E25-08-0412","DOIUrl":"10.1091/mbc.E25-08-0412","url":null,"abstract":"Osteoclast-mediated bone resorption depends on the secretion of lysosomal hydrolases via the fusion of secretory lysosomes with the ruffled border, yet the molecular mechanisms governing lysosomal trafficking and fusion remain incompletely understood. Here, we demonstrate that the small GTPase Arl8b regulates the processing of osteoclast-specific lysosomal hydrolase, cathepsin K, and the positioning of secretory lysosomes toward the actin ring. Accordingly, depletion of Arl8b led to defects in lysosome-mediated bone resorption in osteoclasts. We identify RUFY4 as a RANKL-inducible Arl8b effector that promotes lysosome clustering and maturation by linking Arl8b to Rab7 through the adaptor PLEKHM1 and recruiting the multi-subunit tethering factor HOPS complex to drive late endosome-lysosome fusion. Depletion of RUFY4 or HOPS subunits impairs cathepsin K processing and disrupts lysosome positioning, leading to reduced bone resorption activity. These findings suggest that Arl8b and its interaction partners play essential roles in biogenesis and positioning of secretory lysosomes, essential for osteoclast function in bone remodeling.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"ar43"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147609400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A role for Keratin 17 in Rac1-mediated DNA damage response in keratinocytes. 角蛋白17在角化细胞中rac1介导的DNA损伤反应中的作用。

IF 2.7 3区生物学

Molecular Biology of the Cell Pub Date : 2026-05-01 Epub Date: 2026-03-25 DOI: 10.1091/mbc.E25-05-0238

Christopher Pineda, Erez Cohen, Beau Su, Jiwoo Yeom, Jewoo Kim, Chang-Hun Lee, Pierre A Coulombe

{"title":"A role for Keratin 17 in Rac1-mediated DNA damage response in keratinocytes.","authors":"Christopher Pineda, Erez Cohen, Beau Su, Jiwoo Yeom, Jewoo Kim, Chang-Hun Lee, Pierre A Coulombe","doi":"10.1091/mbc.E25-05-0238","DOIUrl":"10.1091/mbc.E25-05-0238","url":null,"abstract":"Keratin 17 (K17) is a stress-responsive intermediate filament protein that is upregulated in chronic skin diseases and in several carcinomas. We previously showed that K17 is induced in epidermal keratinocytes following exposure to DNA-damaging agents, promoting keratinocyte survival and chemically induced papilloma formation in mouse skin. Molecularly, K17 is recruited to the nucleus, where it impacts nuclear architecture, gene expression, and the DNA damage response (DDR). Here, we report on efforts to delineate K17-dependent processes during DDR by focusing on its interacting partners. Using mass spectrometry, we identified a network of K17-interacting Rho GTPase signaling proteins, including Rac1 and its activator Dock7. Biochemically, we confirmed that Rac1 and K17 interact directly in vitro and in A431 tumor keratinocytes, both at baseline and after ionizing radiation. We show that KRT17 deletion leads to decreased levels of Rac1 protein, its DNA damage-related effector TOP2A, and a Rac1-dependent decrease in cellular proliferation following ionizing radiation. Remarkably, key K17-dependent readouts are rescued by expression of constitutively active, but not dominant-negative, Rac mutants in KRT17 null A431 keratinocytes. These findings uncover a K17-Rac1-TOP2A signaling axis that promotes DDR and associated proliferation, with implications for cancer and chronic skin diseases.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"ar41"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147513123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Steady-state epithelial apical flatness is characterized by MLCK morphodynamics and asynchronous Ca²⁺ oscillations, but not by underlying ECM geometry. 稳态上皮顶端平坦度的特征是MLCK形态动力学和异步Ca2+振荡，但不是潜在的ECM几何。

IF 2.7 3区生物学

Molecular Biology of the Cell Pub Date : 2026-05-01 Epub Date: 2026-04-02 DOI: 10.1091/mbc.E25-12-0583

Hao Wu, Emerson Herrmann, Jeanette Hyer, Lisa Hua, Takashi Mikawa

{"title":"Steady-state epithelial apical flatness is characterized by MLCK morphodynamics and asynchronous Ca2+ oscillations, but not by underlying ECM geometry.","authors":"Hao Wu, Emerson Herrmann, Jeanette Hyer, Lisa Hua, Takashi Mikawa","doi":"10.1091/mbc.E25-12-0583","DOIUrl":"10.1091/mbc.E25-12-0583","url":null,"abstract":"The canonical simple epithelium is a flat sheet-like tissue of horizontally packed cells. While the basal surface is delineated by the basement membrane of extracellular matrix (ECM), little is known about how a flat apical surface is maintained, or if apical/basal dynamics are coordinated. The current study tests the role of the apical domain to define mechanisms involved in maintaining a flat apical geometry in an epithelium. When the basal geometry is modulated, Madin-Darby Canine Kidney (MDCK) cells adjust their morphology to maintain an overall apical flatness of the confluent layer. Pharmacological and transgenic disruption of non-muscle myosin ATPase and MLCK activity results in an uneven apical structure and overall loss of the flat geometry typical of a confluent epithelium. Surprisingly, transgenic experimentation showed that forces maintaining individual MDCK cell flatness are cell-autonomous. Finally, Ca2+ imaging reveals an asynchronous calcium flux across a confluent epithelium. Our results highlight that apical/basal cellular surfaces may not be tightly coordinated, but rather independently regulated. This study provides a new paradigm for how apical flatness is regulated at steady state.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"ar45"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147609363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Anticipatory capture of circulating peptidergic vesicles in a clock neuron. 时钟神经元中循环肽能囊泡的预期捕获。

IF 2.7 3区生物学

Molecular Biology of the Cell Pub Date : 2026-05-01 Epub Date: 2026-03-11 DOI: 10.1091/mbc.E25-11-0558

Markus K Klose, Junghun Kim, Brigitte F Schmidt, David L Deitcher, Edwin S Levitan

{"title":"Anticipatory capture of circulating peptidergic vesicles in a clock neuron.","authors":"Markus K Klose, Junghun Kim, Brigitte F Schmidt, David L Deitcher, Edwin S Levitan","doi":"10.1091/mbc.E25-11-0558","DOIUrl":"10.1091/mbc.E25-11-0558","url":null,"abstract":"Neuropeptide release by Drosophila sLNv clock neurons controls circadian behaviors and sleep. Strikingly, neuropeptide content in sLNv terminals is rhythmic with late-night accumulation occurring, while the axon arbor is expanding in preparation for midmorning synaptic exocytosis of neuropeptide-containing dense-core vesicles (DCV). Past studies showed that increased synaptic neuropeptide content can be produced by delivery of more neuropeptide to terminals or activity-dependent capture of circulating DCVs. To distinguish between these mechanisms, neuropeptide-containing DCVs were imaged in the ex vivo brain explant preparation. First, postexocytosis DCV axonal transport and presynaptic neuropeptide accumulation following retrograde transport inhibition show that sLNv DCVs circulate. Furthermore, anterograde transport to terminals is constant throughout the day demonstrating there is no increase in DCV delivery. Rather, capture of circulating DCVs produces the daily boost in terminal neuropeptide content. Remarkably, this capture occurs before the daily increase in Ca2+ spike activity and is independent of concurrent IP3 signaling and axon arbor expansion. Finally, a per clock gene mutation inhibits rhythmic DCV capture. Thus, rather than responding to Ca2+ signaling or axonal plasticity, capture of circulating DCVs in sLNv presynapses is increased by the molecular clock in anticipation of activity-induced release hours later.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"br12"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147434263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Interplay between membrane protrusive activities and their adhesion strength regulates cell migration. 细胞膜的突出活性与其粘附强度之间的相互作用调节着细胞的迁移。

IF 2.7 3区生物学

Molecular Biology of the Cell Pub Date : 2026-05-01 Epub Date: 2026-03-25 DOI: 10.1091/mbc.E25-12-0621

Indranil Ghosh, Ditipriya Mallick, Ankita Sen, Anwesha Kar, Shilpak Chatterjee, Siddhartha Sankar Jana

{"title":"Interplay between membrane protrusive activities and their adhesion strength regulates cell migration.","authors":"Indranil Ghosh, Ditipriya Mallick, Ankita Sen, Anwesha Kar, Shilpak Chatterjee, Siddhartha Sankar Jana","doi":"10.1091/mbc.E25-12-0621","DOIUrl":"10.1091/mbc.E25-12-0621","url":null,"abstract":"Migratory cells can adopt membrane protrusions like blebbing or lamellipodia for efficient migration. The underlying mechanisms of how switching contributes to cell migration are not clearly understood. Here, we found that nonmuscle myosin II (NM II) mediated blebbing to lamellipodia conversion (BLC) increased the speed of migration, whereas lamellipodia to blebbing conversion (LBC) decreased it in various cells, such as cancerous cells, mesenchymal stem cells, and T-lymphocytes. Cells with lamellipodia had larger and greater numbers of focal adhesions compared with blebbing cells, suggesting a link between adhesion strength and membrane protrusions and migration. Migratory cells seeded on collagen I, but not on poly-L-lysine, exhibited a faster BLC and greater migration speed compared with cells seeded on an uncoated surface. Knockdown of integrinβ1 reduced cell migration, but these cells were able to undergo conversion of membrane protrusions, albeit with a substantial delay. These findings suggest that cells can fine-tune the migration strategy by controlling NM II-mediated protrusion switching and modulating integrin-dependent adhesion strength.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"ar40"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147513459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Breaking the annotation barrier: An initial subcellular localization atlas of Giardia's hypothetical and conserved hypothetical proteins provides a resource for functional discovery. 打破注释障碍：贾第鞭毛虫假设和保守假设蛋白质的初始亚细胞定位图谱为功能发现提供了资源。

IF 2.7 3区生物学

Molecular Biology of the Cell Pub Date : 2026-05-01 Epub Date: 2026-03-25 DOI: 10.1091/mbc.E25-12-0590

Kari D Hagen, Alexander J Zerkle, Satvik Arani, Tiffany Chase, Michael J Cipriano, Matthew P Hirakawa, Jonathan K Pham, David J Woessner, Christopher Nosala, Shane G McInally, Nicholas A Hilton, Joseph A Williams, Kristopher Nguyen, Gregory T Walker, Lorita Boghospor, Allen B Tu, Andrew Bluhm, Sharon Jan, Katie Chun, Gary Du, Albert C Sek, Jacqueline Booker, Scott C Dawson

{"title":"Breaking the annotation barrier: An initial subcellular localization atlas of Giardia's hypothetical and conserved hypothetical proteins provides a resource for functional discovery.","authors":"Kari D Hagen, Alexander J Zerkle, Satvik Arani, Tiffany Chase, Michael J Cipriano, Matthew P Hirakawa, Jonathan K Pham, David J Woessner, Christopher Nosala, Shane G McInally, Nicholas A Hilton, Joseph A Williams, Kristopher Nguyen, Gregory T Walker, Lorita Boghospor, Allen B Tu, Andrew Bluhm, Sharon Jan, Katie Chun, Gary Du, Albert C Sek, Jacqueline Booker, Scott C Dawson","doi":"10.1091/mbc.E25-12-0590","DOIUrl":"10.1091/mbc.E25-12-0590","url":null,"abstract":"Giardia intestinalis is a globally prevalent cause of waterborne diarrheal disease, yet about 40% of its proteome remains functionally uncharacterized due to the lack of conserved homologous proteins and limited experimental validation of protein function. To begin addressing this gap, we created a large-scale subcellular localization resource by fluorescently tagging and imaging 608 Giardia proteins (12% of the proteome) expressed in live cells from native promoters. This dataset includes 240 hypothetical proteins, 215 domain-family proteins (including ankyrin repeat and NEK kinase families), 171 diplomonad- or Giardia-specific proteins, 69 conserved eukaryotic proteins, and 77 proteins with known functions that were previously unlocalized. Imaging revealed localization to cytoskeletal and Giardia-specific organelles (eight flagella, the ventral disk, and the median body), along with novel components of the plasma membrane and endomembrane systems. Integrating localization data with domain architecture, homology, and Giardia-specific Gene Ontology terms, we produced a \"localization-informed\" gene annotation with a standardized, structured nomenclature. This resource provides the largest experimentally validated functional annotation of the Giardia proteome to date, linking predicted gene models to cellular structures, creating testable hypotheses for protein function and establishing a durable framework for future studies of cell biology, pathogenesis, and eukaryotic evolution in this deeply divergent diplomonad lineage.","PeriodicalId":18735,"journal":{"name":"Molecular Biology of the Cell","volume":" ","pages":"mr4"},"PeriodicalIF":2.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147513463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0