Life Science Alliance最新文献_第5页

The APOL1 variant p.N264K is predicted to block ion flow by occluding a pore at the cell surface. 据预测，APOL1变体p.N264K通过堵塞细胞表面的孔来阻断离子流动。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-03-10 Print Date: 2026-05-01 DOI: 10.26508/lsa.202503570

Verena Höffken, Lara Console, Niklas Nelde, Hermann Pavenstädt, Cesare Indiveri, Thomas Weide

{"title":"The APOL1 variant p.N264K is predicted to block ion flow by occluding a pore at the cell surface.","authors":"Verena Höffken, Lara Console, Niklas Nelde, Hermann Pavenstädt, Cesare Indiveri, Thomas Weide","doi":"10.26508/lsa.202503570","DOIUrl":"10.26508/lsa.202503570","url":null,"abstract":"The APOL1 gene variants G1 and G2 are associated with an increased risk of APOL1-mediated kidney disease. A recently identified variant, p.N264K (M1), mitigates this risk of renal damage by abolishing APOL1-G2's associated cytotoxicity. However, the molecular and structural basis of this protective effect remains incompletely understood. In this study, we first show that both the cytotoxic G2 and the nontoxic M1-G2 exhibit similar intracellular localization, surface expression, and turnover kinetics. Moreover, N-glycosylation assays indicated no differences in topology, and 3D models demonstrated that both cytotoxic G2 and nontoxic APOL1 M1-G2 span the membrane four times, forming a potential ion channel. Interestingly, molecular dynamics analyses of a computational APOL1 3D model further revealed that in case of M1, the lysine at position 264 occludes this channel, thereby preventing ion pore activity of APOL1. These findings provide, for the first time, a mechanistic explanation for the nontoxic behavior of the APOL1 M1-G2 variant. Additional 3D analyses suggest that the C-terminal region may contribute to APOL1 multimerization, potentially influencing ion flux and cytotoxicity.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 5","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12976425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147434008","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

The CDKL5 kinase undergoes liquid-liquid phase separation driven by a serine-rich C-terminal region. CDKL5激酶在富含丝氨酸的c端区驱动下进行液液相分离。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-03-10 Print Date: 2026-05-01 DOI: 10.26508/lsa.202503402

Stefania Boggio Bozzo, Marco Dell'Oca, Serena Vaglietti, Antonia Gurgone, Vita Cardinale, Gregorio Ragazzini, Andrea Alessandrini, Luca Colnaghi, J Fernando Bazan, Mirella Ghirardi, Maurizio Giustetto, Ferdinando Fiumara

{"title":"The CDKL5 kinase undergoes liquid-liquid phase separation driven by a serine-rich C-terminal region.","authors":"Stefania Boggio Bozzo, Marco Dell'Oca, Serena Vaglietti, Antonia Gurgone, Vita Cardinale, Gregorio Ragazzini, Andrea Alessandrini, Luca Colnaghi, J Fernando Bazan, Mirella Ghirardi, Maurizio Giustetto, Ferdinando Fiumara","doi":"10.26508/lsa.202503402","DOIUrl":"10.26508/lsa.202503402","url":null,"abstract":"The CDKL5 gene encodes a protein kinase involved in nervous system development and function. Pathogenic variants in this gene can cause a severe neurodevelopmental CDKL5 deficiency disorder (CDD). The CDKL5 protein contains a catalytic N-terminal domain (NTD) and a less characterized C-terminal domain (CTD). We discovered that the CTD is a serine-rich low-complexity region driving liquid-liquid phase separation (LLPS), a biophysical process controlling protein localization and function, by which CDKL5 forms intracellular membraneless condensates. A CTD internal fragment (CTIF) plays a pivotal LLPS-promoting role, along with the distal portion of the protein. In CDD, transcripts carrying pathogenic nonsense or frameshift mutations introducing distal premature termination codons may escape nonsense-mediated decay, producing CDKL5 proteins with a variably truncated CTD. We found that two distal truncations, removing part of the CTIF and the downstream protein tail, significantly reduce CDKL5 LLPS and catalytic function. These findings demonstrate that CDKL5 undergoes LLPS, driven by a CTD region whose loss in distally truncated forms of the protein-by impairing LLPS and functional activity-may play a role in the molecular pathogenesis of CDD.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 5","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12976563/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147434006","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

F-actin organization excludes E-cadherin from the division furrow to ensure cytokinesis fidelity. F-actin组织将e -钙粘蛋白排除在分裂沟之外，以确保细胞分裂的保真度。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-03-05 Print Date: 2026-05-01 DOI: 10.26508/lsa.202603664

Debodyuti Mondal, Megha Rai, Anup Padmanabhan

{"title":"F-actin organization excludes E-cadherin from the division furrow to ensure cytokinesis fidelity.","authors":"Debodyuti Mondal, Megha Rai, Anup Padmanabhan","doi":"10.26508/lsa.202603664","DOIUrl":"10.26508/lsa.202603664","url":null,"abstract":"Maintaining intercellular adhesion during proliferative cell division is essential for ensuring tissue integrity during embryonic development. How these two processes are coordinated in vivo remains poorly understood. During early Caenorhabditis elegans embryonic divisions, the cell adhesion receptor, HMR-1/E-cadherin, is absent from the cytokinetic furrow zone and the newly established cell-cell interface. We investigated mechanisms underlying this spatial exclusion of HMR-1 from the furrow zone. We find that crosslinking and compact alignment of CYK-1/formin-polymerized unbranched actin filaments in the cytokinetic furrow restrict the mobility of HMR-1 into the division zone. Disruption of cortical actin organization through depletion of CYK-1 or myosin/NMY-2 leads to HMR-1 accumulation in the furrow zone, and a concomitant increase in cytokinesis failure. Notably, co-depleting HMR-1 in these embryos rescues the observed cytokinesis failure phenotype. Our findings reveal a reciprocal regulatory relationship between cell adhesion and cell division machinery, essential for precise and timely completion of cytokinesis during embryonic development.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 5","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12967896/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147365291","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

Bridging nanomechanics and bioenergetics of single mitochondria by atomic force microscopy. 原子力显微镜下连接单个线粒体的纳米力学和生物能量学。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-03-05 Print Date: 2026-05-01 DOI: 10.26508/lsa.202503602

Ekaterina O Zorikova, Sabita Chourasia, Irit Rosenhek-Goldian, Sidney R Cohen, Semen V Nesterov, Atan Gross

{"title":"Bridging nanomechanics and bioenergetics of single mitochondria by atomic force microscopy.","authors":"Ekaterina O Zorikova, Sabita Chourasia, Irit Rosenhek-Goldian, Sidney R Cohen, Semen V Nesterov, Atan Gross","doi":"10.26508/lsa.202503602","DOIUrl":"10.26508/lsa.202503602","url":null,"abstract":"Mitochondria orchestrate energy conversion and cell fate, yet label-free approaches that report both functional and physical states at the single-organelle level are nonexistent. Here, we combine atomic force microscopy (AFM) imaging with single-mitochondrion phenotyping by quantifying stiffness, height, and spontaneous low-frequency height fluctuations at the nanoscale. Across respiratory activators, inhibitors, and uncouplers, the integrated 0- to 20-Hz fluctuation power correlates with mitochondrial membrane potential (ΔΨm) and does not covary with changes in mitochondrial height (a proxy for swelling). In liver mitochondria lacking mitochondrial carrier homolog 2 (MTCH2), a regulator of mitochondrial metabolism, dynamics, and apoptosis, AFM reveals a compact, mechanically stiff, high-fluctuation state consistent with hyperpolarization and distinct from inhibited/uncoupled signatures. Extending the assay to mitochondria isolated from mouse embryonic fibroblasts, AFM data can distinguish between genotypes: loss of the mitochondrial pro-fusion proteins mitofusin 1 or 2 (MFN1 or MFN2) yields stiff, low-fluctuation mitochondria with reduced ΔΨm, whereas MTCH2 loss produces stiff, high-fluctuation, high-ΔΨm mitochondria. These three label-free features provide reproducible single-organelle \"fingerprints\" that resolve bioenergetic states and molecular defects and complement fluorescence and respirometry.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 5","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12967895/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147365322","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

Metformin improves RAN protein pathology, alternative splicing, and behavioral phenotypes in SCA8 mice. 二甲双胍改善了SCA8小鼠的RAN蛋白病理、选择性剪接和行为表型。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-03-02 Print Date: 2026-05-01 DOI: 10.26508/lsa.202503555

Lisa El Romano, Setsuki Tsukagoshi, Emily E Davey-Osuch, Ramadan Ajredini, Kamat Manasi, Tala Vr Ortiz, Eduardo Rijos, Nathan J Bourgon, S Elaine Ames, Timothy J Garrett, John D Cleary, Eric T Wang, Laura Pw Ranum

{"title":"Metformin improves RAN protein pathology, alternative splicing, and behavioral phenotypes in SCA8 mice.","authors":"Lisa El Romano, Setsuki Tsukagoshi, Emily E Davey-Osuch, Ramadan Ajredini, Kamat Manasi, Tala Vr Ortiz, Eduardo Rijos, Nathan J Bourgon, S Elaine Ames, Timothy J Garrett, John D Cleary, Eric T Wang, Laura Pw Ranum","doi":"10.26508/lsa.202503555","DOIUrl":"10.26508/lsa.202503555","url":null,"abstract":"Spinocerebellar ataxia type 8 (SCA8) is a member of a group of dominantly inherited, debilitating neurological diseases caused by CAG•CTG expansions for which there are no effective treatments. RAN translation, which was discovered in SCA8, has previously been shown to occur across CAG and CUG expansion transcripts, making treatments for SCA8 potentially relevant to a broad group of diseases, including SCA1, SCA2, SCA3, SCA6, SCA7, SCA12, Huntington's disease, and myotonic dystrophy type 1. In addition, CUG and CAG expansion transcripts have been reported to cause RNA gain-of-function effects. Using SCA8 BAC transgenic mice as a model for CAG•CTG expansion diseases, we now show that metformin improves ambulatory performance using rotarod, DigiGait, and open-field testing. At the molecular level, metformin-treated mice show reduced RAN protein levels and improved splicing, without altering sense or antisense RNA levels. Metformin-treated mice also show decreased neuroinflammation, with reduced astrogliosis and fewer activated microglia. These data provide strong preclinical support for testing metformin in clinical trials for SCA8 and potentially the broader group of CAG•CTG repeat expansion disorders.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 5","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12954051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147344627","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

Reframing "disappointing" data at Life Science Alliance. 重构生命科学联盟“令人失望”的数据。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-03-02 Print Date: 2026-03-01 DOI: 10.26508/lsa.202603674

Tim Fessenden

引用次数: 0

Tissue-specific I-Smad mechanisms revealed by structure-function analysis in Drosophila. 果蝇结构-功能分析揭示组织特异性I-Smad机制。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-02-27 Print Date: 2026-05-01 DOI: 10.26508/lsa.202503445

Ania M Simoncek, Steven J Sviridoff, Joshua N Hays, Noah J Graichen, Mikolaj J Sulkowski

{"title":"Tissue-specific I-Smad mechanisms revealed by structure-function analysis in Drosophila.","authors":"Ania M Simoncek, Steven J Sviridoff, Joshua N Hays, Noah J Graichen, Mikolaj J Sulkowski","doi":"10.26508/lsa.202503445","DOIUrl":"10.26508/lsa.202503445","url":null,"abstract":"Inhibitory Smads (I-Smads) regulate TGF-β/BMP signaling through multiple distinct mechanisms, but whether different tissues preferentially employ specific mechanisms remains unknown. To address this question, we performed structure-function analyses of the Drosophila I-Smad, Dad, and its vertebrate orthologs Smad6 and Smad7 in neural and wing tissues, measuring outputs of BMP signaling in vivo. We identified a 24-amino acid putative DNA-binding domain within the MH1 domain of Dad that is essential for inhibitory function in wing tissue but unessential in neural tissue. Structural analyses revealed that ΔDNA-binding domain disrupts a β-hairpin structure homologous to R-Smad DNA-binding regions. We also found that Dad requires an intact MH1 domain to disrupt wing development, whereas either MH1 or MH2 can independently disrupt BMP signaling in motor neurons. These findings support a model where Dad functions through MH1-mediated transcriptional regulation in wing primordium, but through multiple mechanisms in neurons. Comparative analysis revealed that vertebrate I-Smad orthologs also show tissue-specific activity patterns, with structural predictions suggesting that Smad6 retains ancestral DNA-binding capacity, whereas Smad7 has evolved enhanced MH2-mediated functions. These results reveal context-dependent mechanisms of I-Smads that further the understanding of TGF-β/BMP pathway regulation.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 5","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12948492/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147317455","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

Rnd3 regulates lung cancer cell invasion and migration independently of ROCK1 signaling via alpha 5 integrin modulation. Rnd3通过α 5整合素的调节，独立于ROCK1信号调控肺癌细胞的侵袭和迁移。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-02-24 Print Date: 2026-05-01 DOI: 10.26508/lsa.202503494

Noemi Garcia Garcia, Thanh Ha Vy Nguyen, Dane Richey, Emily F Cox, Jon Coca Juaristi, Cody Ashby, Analiz Rodriguez, Katie R Ryan

{"title":"Rnd3 regulates lung cancer cell invasion and migration independently of ROCK1 signaling via alpha 5 integrin modulation.","authors":"Noemi Garcia Garcia, Thanh Ha Vy Nguyen, Dane Richey, Emily F Cox, Jon Coca Juaristi, Cody Ashby, Analiz Rodriguez, Katie R Ryan","doi":"10.26508/lsa.202503494","DOIUrl":"10.26508/lsa.202503494","url":null,"abstract":"Rnd3 regulates cellular processes commonly dysregulated in cancer, and altered Rnd3 expression has been linked to several cancer types. Here, we show lung adenocarcinoma patients expressing low levels of Rnd3 have significantly higher survival rates. To gain mechanistic insight into this correlation, we knocked down Rnd3 in lung adenocarcinoma A549 and H460 cell lines and patient-derived lung-to-brain metastasis (PDLBM) cell lines as a proxy for advanced disease. Depletion of Rnd3 expression decreases cell invasion and migration, two hallmarks of metastasis, independently of RhoA-ROCK1 signaling in both lung adenocarcinoma and PDLBM cell lines, indicating the involvement of a novel pathway. The expression of alpha 5 integrin was increased in Rnd3-depleted A549 cells, and knocking down alpha 5 integrin restored cell migration and invasion rates in A549 cells. Identification of a RhoA-ROCK1-independent mechanism by which Rnd3 modulates alpha 5 integrin expression to control cell migration and invasion provides new insights into the molecular basis of pro-malignant properties. These properties that drive the metastatic potential of lung adenocarcinoma may be exploited to target metastatic disease.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 5","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12932936/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147284218","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

Unlocking the secrets of SARS-CoV-2 nsp3 by combining experiments with AlphaFold2 domain prediction. 结合实验与AlphaFold2结构域预测揭开SARS-CoV-2 nsp3的秘密。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-02-20 Print Date: 2026-04-01 DOI: 10.26508/lsa.202503247

Maximilian Edich, Yunyun Gao, David C Briggs, Andrea Thorn

{"title":"Unlocking the secrets of SARS-CoV-2 nsp3 by combining experiments with AlphaFold2 domain prediction.","authors":"Maximilian Edich, Yunyun Gao, David C Briggs, Andrea Thorn","doi":"10.26508/lsa.202503247","DOIUrl":"10.26508/lsa.202503247","url":null,"abstract":"Nonstructural protein 3 (nsp3) is crucial for SARS-CoV-2 infection. It is the largest protein of the virus with roughly 2000 residues, and a major drug target. However, because of its size, disordered regions, and transmembrane domains, the atomic structure of the whole protein has not yet been established. Only 10 out of its 16 domains were individually determined in experiments. Here, we demonstrate how structural bioinformatics, AI-based fold prediction, and traditional experiments complement each other and can shed light on the makeup of this important protein, both in SARS-CoV-2 and in related viruses. Our method can be generalized for other multidomain proteins. Our prediction-based approach reveals a previously undescribed folded domain, which we could confirm experimentally. Our research also suggests a potential function of the domain Y1: this domain may be involved in the assembly of nsp3, nsp4, and nsp6 into the hexameric pore, which was discovered by electron tomography and exports RNA into the cytosol. The Y1 hexamer, however, could not be expressed on its own. We revise domain segmentation and nomenclature of nsp3 domains.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12923375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146258707","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

Natural variations in maternal behavior shape anxiety and hippocampal neurogenesis in offspring. 母性行为的自然变异塑造了后代的焦虑和海马神经发生。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-02-19 Print Date: 2026-05-01 DOI: 10.26508/lsa.202503419

Fabio Grieco, Pauline van Gelderen, Maryam Ali, Thomas Larrieu, Nicolas Toni

{"title":"Natural variations in maternal behavior shape anxiety and hippocampal neurogenesis in offspring.","authors":"Fabio Grieco, Pauline van Gelderen, Maryam Ali, Thomas Larrieu, Nicolas Toni","doi":"10.26508/lsa.202503419","DOIUrl":"10.26508/lsa.202503419","url":null,"abstract":"Understanding the mechanisms of individualization of emotional traits is crucial for the development of personalized medicine in mood disorders. Although previous research focused on genetic differences or experimental manipulations of maternal care, it is unclear whether natural variations in maternal care in the absence of genetic variability influence anxiety-related behavior and neurogenesis. We addressed this question by observing inbred mouse maternal care and offspring in a longitudinal manner. We found that mothers spontaneously displaying low maternal care showed lower adult neurogenesis in both the olfactory bulb and the hippocampus compared with high maternal care mothers. In turn, low maternal care-reared pups exhibited increased anxiety as compared to high maternal care-reared pups, which was associated with decreased postnatal neurogenesis after weaning. These results highlight that in the absence of genetic diversity, natural variations in early-life experience are sufficient to shape brain plasticity and anxiety-related behavior in offspring. This underscores the relevance of maternal care and hippocampal neurogenesis in shaping personality-like traits related to mood disorders and inducing emotional individuality in early stages of life.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 5","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12920054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146227286","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