Life Science Alliance最新文献_第8页

Regulation of proteostasis by sleep through autophagy in Drosophila models of Alzheimer's disease. 在阿尔茨海默病果蝇模型中，睡眠通过自噬调节蛋白稳态。

IF 3.3 2区生物学

Life Science Alliance Pub Date : 2024-09-05 Print Date: 2024-11-01 DOI: 10.26508/lsa.202402681

Natalie Ortiz-Vega, Amanda G Lobato, Tijana Canic, Yi Zhu, Stanislav Lazopulo, Sheyum Syed, R Grace Zhai

{"title":"Regulation of proteostasis by sleep through autophagy in Drosophila models of Alzheimer's disease.","authors":"Natalie Ortiz-Vega, Amanda G Lobato, Tijana Canic, Yi Zhu, Stanislav Lazopulo, Sheyum Syed, R Grace Zhai","doi":"10.26508/lsa.202402681","DOIUrl":"10.26508/lsa.202402681","url":null,"abstract":"Sleep and circadian rhythm dysfunctions are common clinical features of Alzheimer's disease (AD). Increasing evidence suggests that in addition to being a symptom, sleep disturbances can also drive the progression of neurodegeneration. Protein aggregation is a pathological hallmark of AD; however, the molecular pathways behind how sleep affects protein homeostasis remain elusive. Here we demonstrate that sleep modulation influences proteostasis and the progression of neurodegeneration in Drosophila models of tauopathy. We show that sleep deprivation enhanced Tau aggregational toxicity resulting in exacerbated synaptic degeneration. In contrast, sleep induction using gaboxadol led to reduced toxic Tau accumulation in neurons as a result of modulated autophagic flux and enhanced clearance of ubiquitinated Tau, suggesting altered protein processing and clearance that resulted in improved synaptic integrity and function. These findings highlight the complex relationship between sleep and regulation of protein homeostasis and the neuroprotective potential of sleep-enhancing therapeutics to slow the progression or delay the onset of neurodegeneration.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 11","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11377308/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142140487","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

A novel role for CSA in the regulation of nuclear envelope integrity: uncovering a non-canonical function. CSA 在调节核包膜完整性中的新作用：发现一种非规范功能。

IF 3.3 2区生物学

Life Science Alliance Pub Date : 2024-08-29 Print Date: 2024-11-01 DOI: 10.26508/lsa.202402745

Denny Yang, Austin Lai, Amelie Davies, Anne Fj Janssen, Matthew O Ellis, Delphine Larrieu

{"title":"A novel role for CSA in the regulation of nuclear envelope integrity: uncovering a non-canonical function.","authors":"Denny Yang, Austin Lai, Amelie Davies, Anne Fj Janssen, Matthew O Ellis, Delphine Larrieu","doi":"10.26508/lsa.202402745","DOIUrl":"10.26508/lsa.202402745","url":null,"abstract":"Cockayne syndrome (CS) is a premature ageing condition characterized by microcephaly, growth failure, and neurodegeneration. It is caused by mutations in ERCC6 or ERCC8 encoding for Cockayne syndrome B (CSB) and A (CSA) proteins, respectively. CSA and CSB have well-characterized roles in transcription-coupled nucleotide excision repair, responsible for removing bulky DNA lesions, including those caused by UV irradiation. Here, we report that CSA dysfunction causes defects in the nuclear envelope (NE) integrity. NE dysfunction is characteristic of progeroid disorders caused by a mutation in NE proteins, such as Hutchinson-Gilford progeria syndrome. However, it has never been reported in Cockayne syndrome. We observed CSA dysfunction affected LEMD2 incorporation at the NE and increased actin stress fibers that contributed to enhanced mechanical stress to the NE. Altogether, these led to NE abnormalities associated with the activation of the cGAS/STING pathway. Targeting the linker of the nucleoskeleton and cytoskeleton complex was sufficient to rescue these phenotypes. This work reveals NE dysfunction in a progeroid syndrome caused by mutations in a DNA damage repair protein, reinforcing the connection between NE deregulation and ageing.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 11","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142116924","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

Mitochondrial double-stranded RNA homeostasis depends on cell-cycle progression. 线粒体双链 RNA 的平衡取决于细胞周期的进展。

IF 3.3 2区生物学

Life Science Alliance Pub Date : 2024-08-29 Print Date: 2024-11-01 DOI: 10.26508/lsa.202402764

Vanessa Xavier, Silvia Martinelli, Ryan Corbyn, Rachel Pennie, Kai Rakovic, Ian R Powley, Leah Officer-Jones, Vincenzo Ruscica, Alison Galloway, Leo M Carlin, Victoria H Cowling, John Le Quesne, Jean-Claude Martinou, Thomas MacVicar

{"title":"Mitochondrial double-stranded RNA homeostasis depends on cell-cycle progression.","authors":"Vanessa Xavier, Silvia Martinelli, Ryan Corbyn, Rachel Pennie, Kai Rakovic, Ian R Powley, Leah Officer-Jones, Vincenzo Ruscica, Alison Galloway, Leo M Carlin, Victoria H Cowling, John Le Quesne, Jean-Claude Martinou, Thomas MacVicar","doi":"10.26508/lsa.202402764","DOIUrl":"10.26508/lsa.202402764","url":null,"abstract":"Mitochondrial gene expression is a compartmentalised process essential for metabolic function. The replication and transcription of mitochondrial DNA (mtDNA) take place at nucleoids, whereas the subsequent processing and maturation of mitochondrial RNA (mtRNA) and mitoribosome assembly are localised to mitochondrial RNA granules. The bidirectional transcription of circular mtDNA can lead to the hybridisation of polycistronic transcripts and the formation of immunogenic mitochondrial double-stranded RNA (mt-dsRNA). However, the mechanisms that regulate mt-dsRNA localisation and homeostasis are largely unknown. With super-resolution microscopy, we show that mt-dsRNA overlaps with the RNA core and associated proteins of mitochondrial RNA granules but not nucleoids. Mt-dsRNA foci accumulate upon the stimulation of cell proliferation and their abundance depends on mitochondrial ribonucleotide supply by the nucleoside diphosphate kinase, NME6. Consequently, mt-dsRNA foci are profuse in cultured cancer cells and malignant cells of human tumour biopsies. Our results establish a new link between cell proliferation and mitochondrial nucleic acid homeostasis.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 11","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108923","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

Differential modulation of polycomb-associated histone marks by cBAF, pBAF, and gBAF complexes. cBAF、pBAF 和 gBAF 复合物对多聚酶相关组蛋白标记的不同调节。

IF 3.3 2区生物学

Life Science Alliance Pub Date : 2024-08-29 Print Date: 2024-11-01 DOI: 10.26508/lsa.202402715

Mary Bergwell, JinYoung Park, Jacob G Kirkland

{"title":"Differential modulation of polycomb-associated histone marks by cBAF, pBAF, and gBAF complexes.","authors":"Mary Bergwell, JinYoung Park, Jacob G Kirkland","doi":"10.26508/lsa.202402715","DOIUrl":"10.26508/lsa.202402715","url":null,"abstract":"Chromatin regulators alter the physical properties of chromatin to make it more or less permissive to transcription by modulating another protein's access to a specific DNA sequence through changes in nucleosome occupancy or histone modifications at a particular locus. Mammalian SWI/SNF complexes are a group of ATPase-dependent chromatin remodelers. In mouse embryonic stem cells, there are three primary forms of mSWI/SNF: canonical BAF (cBAF), polybromo-associated BAF (pBAF), and GLTSCR-associated BAF (gBAF). Nkx2-9 is bivalent, meaning nucleosomes at the locus have active and repressive modifications. In this study, we used unique BAF subunits to recruit each of the three complexes to Nkx2-9 using dCas9-mediated inducible recruitment (FIRE-Cas9). We show that recruitment of cBAF complexes leads to a significant loss of the polycomb repressive-2 H3K27me3 histone mark and polycomb repressive-1 and repressive-2 complex proteins, whereas gBAF and pBAF do not. Moreover, nucleosome occupancy alone cannot explain the loss of these marks. Our results demonstrate that cBAF has a unique role in the direct opposition of polycomb-associated histone modifications that gBAF and pBAF do not share.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 11","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108922","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

Retraction: Chitinase 1 regulates pulmonary fibrosis by modulating TGF-β/SMAD7 pathway via TGFBRAP1 and FOXO3. 撤回：几丁质酶1通过TGFBRAP1和FOXO3调节TGF-β/SMAD7通路，从而调控肺纤维化

IF 3.3 2区生物学

Life Science Alliance Pub Date : 2024-08-29 Print Date: 2024-11-01 DOI: 10.26508/lsa.202402987

Chang-Min Lee, Chuan-Hua He, Jin Wook Park, Jae Hyun Lee, Suchitra Kamle, Bing Ma, Bedia Akosman, Roberto Cortez, Emily Chen, Yang Zhou, Erica L Herzog, Changwan Ryu, Xueyan Peng, Ivan O Rosas, Sergio Poli, Carol Feghali Bostwick, Augustine M Choi, Jack A Elias, Chun Geun Lee

引用次数: 0

Cryo-EM reveals a phosphorylated R-domain envelops the NBD1 catalytic domain in an ABC transporter. 冷冻电镜显示，磷酸化的 R-结构域包裹着 ABC 转运体中的 NBD1 催化结构域。

IF 3.3 2区生物学

Life Science Alliance Pub Date : 2024-08-29 Print Date: 2024-11-01 DOI: 10.26508/lsa.202402779

Rodolpho Souza Amado de Carvalho, Md Shamiul Islam Rasel, Nitesh K Khandelwal, Thomas M Tomasiak

{"title":"Cryo-EM reveals a phosphorylated R-domain envelops the NBD1 catalytic domain in an ABC transporter.","authors":"Rodolpho Souza Amado de Carvalho, Md Shamiul Islam Rasel, Nitesh K Khandelwal, Thomas M Tomasiak","doi":"10.26508/lsa.202402779","DOIUrl":"10.26508/lsa.202402779","url":null,"abstract":"Many ATP-binding cassette transporters are regulated by phosphorylation on long and disordered loops which presents a challenge to visualize with structural methods. We have trapped an activated state of the regulatory domain (R-domain) of yeast cadmium factor 1 (Ycf1) by enzymatically enriching the phosphorylated state. A 3.23 Å cryo-EM structure reveals an R-domain structure with four phosphorylated residues and the position for the entire R-domain. The structure reveals key R-domain interactions including a bridging interaction between NBD1 and NBD2 and an interaction with the R-insertion, another regulatory region. We scanned these interactions by systematically replacing segments along the entire R-domain with scrambled combinations of alanine, glycine, and glutamine and probing function under cellular conditions that require the Ycf1 function. We find a close match with these interactions and interacting regions on our R-domain structure that points to the importance of most well-structured segments for function. We propose a model where the R-domain stabilizes a transport-competent state upon phosphorylation by enveloping NBD1 entirely.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 11","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11361370/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108921","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

Helicobacter pylori induces the expression of Lgr5 and stem cell properties in gastric target cells. 幽门螺杆菌诱导胃靶细胞表达 Lgr5 和干细胞特性。

IF 3.3 2区生物学

Life Science Alliance Pub Date : 2024-08-27 Print Date: 2024-11-01 DOI: 10.26508/lsa.202402783

Zuzana Nascakova, Jiazhuo He, Giovanni Papa, Biel Francas, Flora Azizi, Anne Müller

{"title":"Helicobacter pylori induces the expression of Lgr5 and stem cell properties in gastric target cells.","authors":"Zuzana Nascakova, Jiazhuo He, Giovanni Papa, Biel Francas, Flora Azizi, Anne Müller","doi":"10.26508/lsa.202402783","DOIUrl":"10.26508/lsa.202402783","url":null,"abstract":"Helicobacter pylori infection predisposes carriers to a high risk of developing gastric cancer. The cell-of-origin of antral gastric cancer is the Lgr5+ stem cell. Here, we show that infection of antrum-derived gastric organoid cells with H. pylori increases the expression of the stem cell marker Lgr5 as determined by immunofluorescence microscopy, qRT-PCR, and Western blotting, both when cells are grown and infected as monolayers and when cells are exposed to H. pylori in 3D structures. H. pylori exposure increases stemness properties as determined by spheroid formation assay. Lgr5 expression and the acquisition of stemness depend on a functional type IV secretion system (T4SS) and at least partly on the T4SS effector CagA. The pharmacological inhibition or genetic ablation of NF-κB reverses the increase in Lgr5 and spheroid formation. Constitutively active Wnt/β-catenin signaling because of Apc inactivation exacerbates H. pylori-induced Lgr5 expression and stemness, both of which persist even after eradication of the infection. The combined data indicate that H. pylori has stemness-inducing properties that depend on its ability to activate NF-κB signaling.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 11","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11350067/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080792","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

Reprogramming of breast tumor-associated macrophages with modulation of arginine metabolism. 通过调节精氨酸代谢对乳腺肿瘤相关巨噬细胞进行重编程。

IF 3.3 2区生物学

Life Science Alliance Pub Date : 2024-08-27 Print Date: 2024-11-01 DOI: 10.26508/lsa.202302339

Veani Fernando, Xunzhen Zheng, Vandana Sharma, Osama Sweef, Eun-Seok Choi, Saori Furuta

{"title":"Reprogramming of breast tumor-associated macrophages with modulation of arginine metabolism.","authors":"Veani Fernando, Xunzhen Zheng, Vandana Sharma, Osama Sweef, Eun-Seok Choi, Saori Furuta","doi":"10.26508/lsa.202302339","DOIUrl":"10.26508/lsa.202302339","url":null,"abstract":"HER2+ breast tumors have abundant immune-suppressive cells, including M2-type tumor-associated macrophages (TAMs). Although TAMs consist of the immune-stimulatory M1 type and immune-suppressive M2 type, the M1/M2-TAM ratio is reduced in immune-suppressive tumors, contributing to their immunotherapy refractoriness. M1- versus M2-TAM formation depends on differential arginine metabolism, where M1-TAMs convert arginine to nitric oxide (NO) and M2-TAMs convert arginine to polyamines (PAs). We hypothesize that such distinct arginine metabolism in M1- versus M2-TAMs is attributed to different availability of BH4 (NO synthase cofactor) and that its replenishment would reprogram M2-TAMs to M1-TAMs. Recently, we reported that sepiapterin (SEP), the endogenous BH4 precursor, elevates the expression of M1-TAM markers within HER2+ tumors. Here, we show that SEP restores BH4 levels in M2-like macrophages, which then redirects arginine metabolism to NO synthesis and converts M2 type to M1 type. The reprogrammed macrophages exhibit full-fledged capabilities of antigen presentation and induction of effector T cells to trigger immunogenic cell death of HER2+ cancer cells. This study substantiates the utility of SEP in the metabolic shift of the HER2+ breast tumor microenvironment as a novel immunotherapeutic strategy.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 11","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11350068/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080794","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

Identification of single-cell blasts in pediatric acute myeloid leukemia using an autoencoder. 利用自动编码器识别小儿急性髓性白血病中的单细胞突变。

IF 3.3 2区生物学

Life Science Alliance Pub Date : 2024-08-27 Print Date: 2024-11-01 DOI: 10.26508/lsa.202402674

Alice Driessen, Susanne Unger, An-Phi Nguyen, Rhonda E Ries, Soheil Meshinchi, Stefanie Kreutmair, Chiara Alberti, Pavel Sumazin, Richard Aplenc, Michele S Redell, Burkhard Becher, María Rodríguez Martínez

{"title":"Identification of single-cell blasts in pediatric acute myeloid leukemia using an autoencoder.","authors":"Alice Driessen, Susanne Unger, An-Phi Nguyen, Rhonda E Ries, Soheil Meshinchi, Stefanie Kreutmair, Chiara Alberti, Pavel Sumazin, Richard Aplenc, Michele S Redell, Burkhard Becher, María Rodríguez Martínez","doi":"10.26508/lsa.202402674","DOIUrl":"10.26508/lsa.202402674","url":null,"abstract":"Pediatric acute myeloid leukemia (AML) is an aggressive blood cancer with a poor prognosis and high relapse rate. Current challenges in the identification of immunotherapy targets arise from patient-specific blast immunophenotypes and their change during disease progression. To overcome this, we present a new computational research tool to rapidly identify malignant cells. We generated single-cell flow cytometry profiles of 21 pediatric AML patients with matched samples at diagnosis, remission, and relapse. We coupled a classifier to an autoencoder for anomaly detection and classified malignant blasts with 90% accuracy. Moreover, our method assigns a developmental stage to blasts at the single-cell level, improving current classification approaches based on differentiation of the dominant phenotype. We observed major immunophenotype and developmental stage alterations between diagnosis and relapse. Patients with KMT2A rearrangement had more profound changes in their blast immunophenotypes at relapse compared to patients with other molecular features. Our method provides new insights into the immunophenotypic composition of AML blasts in an unbiased fashion and can help to define immunotherapy targets that might improve personalized AML treatment.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 11","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11358707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080793","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

mTORC1 hampers Hedgehog signaling in Tsc2 deficient cells. 在缺乏 Tsc2 的细胞中，mTORC1 阻碍了刺猬信号的传递。

IF 3.3 2区生物学

Life Science Alliance Pub Date : 2024-08-26 Print Date: 2024-11-01 DOI: 10.26508/lsa.202302419

Lasse Jonsgaard Larsen, Elsebet Østergaard, Lisbeth Birk Møller

{"title":"mTORC1 hampers Hedgehog signaling in Tsc2 deficient cells.","authors":"Lasse Jonsgaard Larsen, Elsebet Østergaard, Lisbeth Birk Møller","doi":"10.26508/lsa.202302419","DOIUrl":"10.26508/lsa.202302419","url":null,"abstract":"The mTORC1-complex is negatively regulated by TSC1 and TSC2. Activation of Hedgehog signaling is strictly dependent on communication between Smoothened and the Hedgehog-signaling effector and transcription factor, GLI2, in the primary cilium. Details about this communication are not known, and we wanted to explore this further. Here we report that in Tsc2 -/- MEFs constitutively activated mTORC1 led to mis-localization of Smoothened to the plasma membrane, combined with increased concentration of GLI2 in the cilia and reduced Hedgehog signaling, measured by reduced expression of the Hedgehog target gene, Gli1 Inhibition of mTORC1 rescued the cellular localization of Smoothened to the cilia, reduced the cilia concentration of GLI2, and restored Hedgehog signaling. Our results reveal evidence for a two-step activation process of GLI2. The first step includes GLI2 stabilization and cilium localization, whereas the second step includes communication with cilia-localized Smoothened. We found that mTORC1 inhibits the second step. This is the first demonstration that mTORC1 is involved in the regulation of Hedgehog signaling.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 11","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11349048/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142073215","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