Life Science Alliance最新文献_第3页

UBA3 reduction sensitizes cancer cells to NAE inhibitors. UBA3还原使癌细胞对NAE抑制剂敏感。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-04-29 Print Date: 2026-07-01 DOI: 10.26508/lsa.202503589

Yu-Ling Miao, Li-Na Zhou, Shan-Shan Song, Xu-Bin Bao, Xia-Juan Huan, Jian Ding, Jin-Xue He

{"title":"UBA3 reduction sensitizes cancer cells to NAE inhibitors.","authors":"Yu-Ling Miao, Li-Na Zhou, Shan-Shan Song, Xu-Bin Bao, Xia-Juan Huan, Jian Ding, Jin-Xue He","doi":"10.26508/lsa.202503589","DOIUrl":"10.26508/lsa.202503589","url":null,"abstract":"The NEDD8-activating enzyme (NAE), comprising NAE1 and UBA3, is an anticancer target. The relative contribution of each of these subunits toward NAE inhibitor (NAEi) efficacy remains unclear. We demonstrated a profound interdependence of NAE1 and UBA3 expression. UBA3 reduction augmented NAEi sensitivity, whereas its overexpression led to decreased sensitivity. UBA3 deficiency enhanced RKO xenograft sensitivity to SOMCL-19-133 (NAEi), which was reversed by UBA3 restoration. Cells with naturally low UBA3 expression were highly NAEi-sensitive. The criticality of UBA3 in NAEi sensitivity is not completely unexpected given that the ability of NAEi to directly bind to UBA3 is known. TCGA data showed that rectum adenocarcinoma patients with low UBA3 mRNA had poorer prognoses, and 27.16% of tumors expressed low UBA3 mRNA. We propose that low UBA3 expression may serve as a NAEi sensitivity biomarker, particularly given that MLN4924 (NAEi) phase 3 failures may be due to a lack of patient stratification. Therefore, our key findings, on the criticality of UBA3 in NAEi sensitivity, underpin future clinical evaluations.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 7","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13129363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147775485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

An optimum rate of microtubule flux for error correction in metaphase spindle. 中期纺锤体误差校正的最佳微管通量率。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-04-27 Print Date: 2026-07-01 DOI: 10.26508/lsa.202503612

Yao Wang, Jie Wang, Yu-Ru Liu, Peng-Ye Wang, Ping Xie

引用次数: 0

Convergent transcriptomic signature in iPSC-dopaminergic neurons of hereditary Parkinson's disease. 遗传性帕金森病ipsc -多巴胺能神经元的趋同转录组特征

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-04-24 Print Date: 2026-07-01 DOI: 10.26508/lsa.202503551

Irina V Kopylova, Artem B Ivanov, Lev R Eidelman, Ekaterina N Zaitseva, Ekaterina D Kulikova, Dmitriy A Grehnyov, Alexandra N Bogomazova, Vladimir A Vigont, Elena V Kaznacheyeva, Maria A Lagarkova, Olga S Lebedeva, Evgenii I Olekhnovich

{"title":"Convergent transcriptomic signature in iPSC-dopaminergic neurons of hereditary Parkinson's disease.","authors":"Irina V Kopylova, Artem B Ivanov, Lev R Eidelman, Ekaterina N Zaitseva, Ekaterina D Kulikova, Dmitriy A Grehnyov, Alexandra N Bogomazova, Vladimir A Vigont, Elena V Kaznacheyeva, Maria A Lagarkova, Olga S Lebedeva, Evgenii I Olekhnovich","doi":"10.26508/lsa.202503551","DOIUrl":"10.26508/lsa.202503551","url":null,"abstract":"The clinical and genetic diversity of Parkinson's disease (PD) makes it challenging to identify common mechanisms across different forms. To search for such shared pathways, we performed transcriptomic analysis of iPSC-derived dopaminergic neurons from patients with LRRK2 or Parkin mutations. We discovered a convergent gene expression signature in both genetic backgrounds, indicating a shift away from developmental and proliferative programs (e.g., Wnt/β-catenin signaling, cell cycle) and toward pathways of mature neuronal function (e.g., synaptic transmission, potassium channels). This shift was particularly pronounced in LRRK2 neurons, which showed enhanced markers of synaptic maturation. Concurrently, PD neurons exhibited down-regulation of gene programs supporting axon growth and structural development and upregulated TRAIL (TNF-related apoptosis-inducing ligand) apoptotic pathway. Our findings suggest that in these hereditary forms of PD, distinct mutations may propel neurons toward a similar state of premature specialization coupled with impaired structural development and increased vulnerability, revealing a potential common path in disease pathogenesis.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 7","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13109591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147775478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Flamenco plasticity tunes somatic piRNAs and rewires isoforms, with implications for heritable transposon spread. 弗拉门戈可塑性调节体细胞pirna和重新连接异构体，与遗传转座子传播的含义。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-04-20 Print Date: 2026-07-01 DOI: 10.26508/lsa.202603650

Mai Moritoh, Chikara Takeuchi, Yurika Namba, Hidenori Nishihara, Shigeki Hirakata, Chie Owa, Shinichi Morishita, Yuka W Iwasaki, Mikiko C Siomi

{"title":"Flamenco plasticity tunes somatic piRNAs and rewires isoforms, with implications for heritable transposon spread.","authors":"Mai Moritoh, Chikara Takeuchi, Yurika Namba, Hidenori Nishihara, Shigeki Hirakata, Chie Owa, Shinichi Morishita, Yuka W Iwasaki, Mikiko C Siomi","doi":"10.26508/lsa.202603650","DOIUrl":"10.26508/lsa.202603650","url":null,"abstract":"Transposons drive genome innovation, yet how they evade somatic piRNA defenses, reach the germline, and rewire host genes with limited cost remain unclear. Using comparative long-read sequencing in cultured Drosophila ovarian somatic cells, we show that the long terminal repeat transposon Springer modulates host gene expression through promoter-proximal intronic insertions at an AT-rich motif. Its 5' long terminal repeat initiates transcription that splices into downstream host exons, expanding isoform diversity without adding coding sequence. We catalog 72 Springer-driven isoforms, highlighting its broad mutagenic potential. In parallel, we find that the Flamenco (Flam) uni-strand piRNA cluster, the principal source of somatic piRNAs, undergoes structural remodeling in ovarian somatic cells, replacing antisense transposon fragments with forward-oriented copies. This remodeling reshapes piRNA populations and erodes silencing of specific elements, including Springer This relaxation of somatic repression may create conditions permissive for continued transposon activity, with possible broader implications for genome change. Our findings suggest that Flam plasticity can couple transposon activity to genome rewiring, with potential evolutionary consequences.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 7","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097621/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147729422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

miR-133a-3p and miR-338-3p shape neural crest derivatives in zebrafish. miR-133a-3p和miR-338-3p在斑马鱼中形成神经嵴衍生物。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-04-17 Print Date: 2026-07-01 DOI: 10.26508/lsa.202503431

Tomás J Steeman, Mercedes Torres, Andrea Mj Weiner, Juan A Rubiolo, Laura E Sánchez, Gabriela Coux, Nora B Calcaterra

{"title":"miR-133a-3p and miR-338-3p shape neural crest derivatives in zebrafish.","authors":"Tomás J Steeman, Mercedes Torres, Andrea Mj Weiner, Juan A Rubiolo, Laura E Sánchez, Gabriela Coux, Nora B Calcaterra","doi":"10.26508/lsa.202503431","DOIUrl":"10.26508/lsa.202503431","url":null,"abstract":"Neural crest cells are a transient, multipotent population that gives rise to diverse structures during vertebrate embryonic development, including craniofacial cartilage and pigment cells. Although the transcriptional regulation of neural crest development is well characterized, the role of microRNAs remains less understood. Using a double-transgenic zebrafish model expressing fluorescent reporters under the sox10 promoter, combined with fluorescence-activated cell sorting and RNA sequencing, we identified microRNAs enriched in neural crest cells. We focused on miR-133a-3p and miR-338-3p, previously linked to tumor suppression, to explore their developmental roles. The overexpression of either microRNA led to craniofacial cartilage malformations and reduced melanophore number, accompanied by decreased expression of key regulators including sox9b, sox10, and runx3 Reporter assays confirmed direct targeting of the sox9b 3'untranslated region. In addition, miR-338-3p overexpression increased neural crest cell numbers, suggesting a role in proliferation. These findings uncover novel functions for miR-133a-3p and miR-338-3p in vertebrate craniofacial and pigment cell development, highlighting shared regulatory features between embryogenesis and tumorigenesis.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 7","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090132/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147717161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Metabolite import by SLC33A1 is required for ATF6 activation during endoplasmic reticulum stress. 在内质网应激过程中，ATF6的激活需要SLC33A1输入代谢物。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-04-17 Print Date: 2026-06-01 DOI: 10.26508/lsa.202603679

Ginto George, Heather P Harding, Richard Kay, David Ron, Adriana Ordoñez

{"title":"Metabolite import by SLC33A1 is required for ATF6 activation during endoplasmic reticulum stress.","authors":"Ginto George, Heather P Harding, Richard Kay, David Ron, Adriana Ordoñez","doi":"10.26508/lsa.202603679","DOIUrl":"10.26508/lsa.202603679","url":null,"abstract":"The transcription factor ATF6α has a central role in adapting mammalian cells to ER stress via the unfolded protein response (UPR), prompting efforts to identify ATF6α modulators. Here, an unbiased genome-wide CRISPR-Cas9 screen performed in Chinese Hamster Ovary cells revealed that proteolytic processing of the ATF6α precursor to its active form was impaired in cells lacking the ER-resident solute carrier SLC33A1, a transporter previously implicated in acetyl-CoA import, sialylation, and Nε-lysine protein acetylation. Cells lacking SLC33A1 constitutively trafficked the ATF6α to the Golgi but exhibited impaired Golgi processing and activating proteolysis. IRE1α signalling was derepressed by SLC33A1 deficiency consistent with selective loss of ATF6α-mediated negative feedback in the UPR. Slc33a1-deleted cells accumulated unmodified sialylated N-glycans, precursors to acetylated glycans, likely reflecting impaired glycan processing. Deletion of ER-localised acetyltransferases NAT8 and NAT8B, which catalyse protein Nε-lysine acetylation in the secretory pathway, did not replicate the ATF6α processing defects observed in Slc33a1-deficient cells. Together, our findings highlight a role of SLC33A1-mediated metabolite transport in the post-ER ATF6α maturation, linking small-molecule metabolism to branch-specific signalling in the UPR.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 6","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147717217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Scalable workflows for high-throughput respirometry. 用于高通量呼吸测量的可扩展工作流程。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-04-15 Print Date: 2026-06-01 DOI: 10.26508/lsa.202503446

Corey A Osto, Eugene V Mosharov, Ayelet M Rosenberg, Martin Picard, Linsey Stiles, Orian Shirihai

{"title":"Scalable workflows for high-throughput respirometry.","authors":"Corey A Osto, Eugene V Mosharov, Ayelet M Rosenberg, Martin Picard, Linsey Stiles, Orian Shirihai","doi":"10.26508/lsa.202503446","DOIUrl":"10.26508/lsa.202503446","url":null,"abstract":"Mitochondrial respirometry, the measurement of oxygen consumption rate (OCR) by the electron transport chain (ETC), is a cornerstone of mitochondrial biology and the gold standard for measurements of mitochondrial function. However, existing respirometry methodologies are poorly suited for large-scale studies and high-throughput applications, ultimately limiting the applicability of these methods. This limitation necessitates new methodologies, which are more easily scaled as mitochondrial studies become more complex and diverse. In this study, we detail a respirometry approach we have developed for high-throughput applications including optimized plate layouts, volume-based sample normalization, robust control selection, and automated data processing and quality control. Furthermore, we validate these methodologies across a respirometry study running 703 human brain samples, totaling more than 10,000 data points, which underwent our automated data processing and quality control techniques. Our workflow streamlines assay preparation, execution, and analysis to make respirometry scalable, while reducing operator burden and preserving data integrity. With this study, we provide a transferable blueprint for high-throughput respirometry as the mitochondrial biology field and the studies within it continue to expand in scale.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 6","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13084159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Locally synthesized glycyl aminoacyl-tRNA synthetase is important for local translation in neurons. 局部合成的甘氨酰基trna合成酶在神经元的局部翻译中起着重要的作用。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-04-15 Print Date: 2026-06-01 DOI: 10.26508/lsa.202603630

Tyler Brent de Leon, Adi Golani-Armon, Bar Cohen, Yoav S Arava

{"title":"Locally synthesized glycyl aminoacyl-tRNA synthetase is important for local translation in neurons.","authors":"Tyler Brent de Leon, Adi Golani-Armon, Bar Cohen, Yoav S Arava","doi":"10.26508/lsa.202603630","DOIUrl":"10.26508/lsa.202603630","url":null,"abstract":"Regulation of gene expression is essential for neuronal development and function. A prominent regulatory mechanism involves synthesis of proteins at their activity site. Such local protein synthesis enables neurons to respond rapidly and tightly to stimuli. Key components of the translation machinery, including mRNA and ribosomes, were identified in subcellular regions of neurons. Yet, the role of tRNAs and their charging enzymes, aminoacyl-tRNA synthetases (ARS), in this process remains largely unclear. Here, we demonstrate that glycyl-tRNA synthetase (Gars1) mRNA is abundant in neurites and undergoes local translation, producing GARS1 protein. Notably, Gars1 mRNA colocalizes with mitochondria in a translation-dependent manner, with its coding sequence (CDS) sufficient to direct this association. The localized GARS1 protein is in close proximity to tRNAGly, and disrupting their proximity impairs local protein synthesis in neurites. These findings establish the functional importance of GARS1 and tRNAGly in neuritic translation and highlight mitochondria as hubs for mRNA transport and translation.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 6","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13084160/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

BATF3 regulates differentiation of CD8⁺ T lymphocytes and memory differentiation program. BATF3调节CD8+ T淋巴细胞的分化和记忆分化程序。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-04-13 Print Date: 2026-07-01 DOI: 10.26508/lsa.202503550

Koji Umemura, Yasuhiro Kojima, Jakrawadee Julamanee, Yusuke Okuno, Yuki Takeuchi, Fumiya Ohara, Shihomi Kuwano, Yoshitaka Adachi, Ryo Hanajiri, Seitaro Terakura, Hitoshi Kiyoi

{"title":"BATF3 regulates differentiation of CD8+ T lymphocytes and memory differentiation program.","authors":"Koji Umemura, Yasuhiro Kojima, Jakrawadee Julamanee, Yusuke Okuno, Yuki Takeuchi, Fumiya Ohara, Shihomi Kuwano, Yoshitaka Adachi, Ryo Hanajiri, Seitaro Terakura, Hitoshi Kiyoi","doi":"10.26508/lsa.202503550","DOIUrl":"10.26508/lsa.202503550","url":null,"abstract":"CD8+ T lymphocytes differentiate from effector to memory cells after antigen clearance, with prolonged IL-2 production characterizing functional cytotoxic T lymphocytes (CTLs). To identify transcription factors associated with sustained IL-2 production, we compared influenza virus-specific and cytomegalovirus-specific CTLs, identifying Basic Leucine Zipper ATF-Like Transcription Factor 3 (BATF3) as a key candidate. BATF3 overexpression significantly enhanced cell proliferation in both virus-specific CTLs and CD19 chimeric antigen receptor T (CAR-T) cells while reducing cytokine production. Among AP-1 transcription factor family members, BATF and BATF3 demonstrated similar functions during effector phase expansion, but BATF3 exhibited distinct roles in promoting memory cell formation. ATAC-seq analysis revealed that BATF3 overexpression dynamically regulates chromatin accessibility, affecting diverse cellular processes including cytoskeletal organization, metabolic pathways, and survival signaling. BATF and BATF3 showed comparable kinetics until peak expansion, but BATF3 specifically facilitated the transition from effector to memory phase, up-regulating memory-associated genes while down-regulating exhaustion markers. These findings establish BATF3 as a master regulator of CD8+ T-cell fate determination through chromatin remodeling, offering therapeutic targets for enhancing CAR-T cell persistence in immunotherapy.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 7","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13080723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147674843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Aortic carboxypeptidase-like protein potentiates β1 integrin signaling in mesenchymal progenitors. 主动脉羧基肽酶样蛋白增强间充质祖细胞中β1整合素信号。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-04-08 Print Date: 2026-06-01 DOI: 10.26508/lsa.202503600

Cheyanne L Frosti, Diana Yeritsyan, Matthew D Layne

{"title":"Aortic carboxypeptidase-like protein potentiates β1 integrin signaling in mesenchymal progenitors.","authors":"Cheyanne L Frosti, Diana Yeritsyan, Matthew D Layne","doi":"10.26508/lsa.202503600","DOIUrl":"10.26508/lsa.202503600","url":null,"abstract":"Fibrosis is a pathological process characterized by persistent fibroblast activation and excessive ECM accumulation. Aortic carboxypeptidase-like protein (ACLP), a secreted ECM protein that binds fibrillar collagen, is up-regulated in fibrotic tissues and promotes fibroblast differentiation through canonical TGFβ receptor signaling. We hypothesized that when presented within the collagen matrix, ACLP would engage integrin-dependent mechanical signaling pathways that contribute to fibrogenic activation. Using 10T1/2 mouse mesenchymal progenitor cells, we identify a previously unrecognized mechanism through which collagen-bound ACLP induces fibrogenic activation via β1 integrin-mediated signaling. Collagen-bound ACLP induced rapid cell spreading, increased β1 integrin activation, and promoted focal adhesion maturation. These adhesion events triggered activation of the GTPases RhoA and Rac1, accompanied by enhanced F-actin assembly and nuclear accumulation of myocardin-related transcription factor A, a key regulator of fibrogenic gene expression. Transcriptomic profiling revealed enrichment of focal adhesion, ECM-receptor interaction, and actin cytoskeletal pathways downstream of collagen-bound ACLP, which was conserved in primary adipose-derived stromal cells. Together, these findings establish collagen-bound ACLP as a matrix-derived cue that links ECM composition to integrin-dependent fibrogenic activation.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 6","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13062534/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0