Molecular and Cellular Biology最新文献_第7页

The DNA Damage Repair Function of Fission Yeast CK1 Involves Targeting Arp8, a Subunit of the INO80 Chromatin Remodeling Complex. 裂殖酵母 CK1 的 DNA 损伤修复功能涉及靶向 INO80 染色质重塑复合物的一个亚基 Arp8。

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2024-01-01 Epub Date: 2024-10-10 DOI: 10.1080/10985549.2024.2408016

Sierra N Cullati, Kazutoshi Akizuki, Yufan Shan, Eric Zhang, Liping Ren, Rodrigo X Guillen, Lesley A Turner, Jun-Song Chen, Jose Navarrete-Perea, Zachary C Elmore, Steven P Gygi, Kathleen L Gould

{"title":"The DNA Damage Repair Function of Fission Yeast CK1 Involves Targeting Arp8, a Subunit of the INO80 Chromatin Remodeling Complex.","authors":"Sierra N Cullati, Kazutoshi Akizuki, Yufan Shan, Eric Zhang, Liping Ren, Rodrigo X Guillen, Lesley A Turner, Jun-Song Chen, Jose Navarrete-Perea, Zachary C Elmore, Steven P Gygi, Kathleen L Gould","doi":"10.1080/10985549.2024.2408016","DOIUrl":"10.1080/10985549.2024.2408016","url":null,"abstract":"The CK1 family are conserved serine/threonine kinases with numerous substrates and cellular functions. The fission yeast CK1 orthologues Hhp1 and Hhp2 were first characterized as regulators of DNA repair, but the mechanism(s) by which CK1 activity promotes DNA repair had not been investigated. Here, we found that deleting Hhp1 and Hhp2 or inhibiting CK1 catalytic activities in yeast or in human cells increased double-strand breaks (DSBs). The primary pathways to repair DSBs, homologous recombination and nonhomologous end joining, were both less efficient in cells lacking Hhp1 and Hhp2 activity. To understand how Hhp1 and Hhp2 promote DNA damage repair, we identified new substrates of these enzymes using quantitative phosphoproteomics. We confirmed that Arp8, a component of the INO80 chromatin remodeling complex, is a bona fide substrate of Hhp1 and Hhp2 important for DNA repair. Our data suggest that Hhp1 and Hhp2 facilitate DNA repair by phosphorylating multiple substrates, including Arp8.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"562-576"},"PeriodicalIF":3.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11583621/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470012","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

Active Gαi/o Mutants Accelerate Breast Tumor Metastasis via the c-Src Pathway 活性 Gαi/o 突变体通过 c-Src 通路加速乳腺肿瘤转移

IF 5.3 2区生物学

Molecular and Cellular Biology Pub Date : 2023-12-15 DOI: 10.1080/10985549.2023.2285833

Cancan LyuAarzoo K. BhimaniWilliam T. DrausRonald WeigelSonghai Chena The Department of Neuroscience and Pharmacology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa, USAb The Department of Surgery, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa, USAc The Holden Comprehensive Cancer Center, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

引用次数: 0

Eukaryotic Clathrin Adapter Protein and Mediator of Cholesterol Homeostasis, PICALM, Affects Trafficking to the Chlamydial Inclusion. 真核克拉色林适配蛋白和胆固醇稳态调解因子 PICALM 影响衣原体包涵体的通路。

IF 5.3 2区生物学

Molecular and Cellular Biology Pub Date : 2023-02-13 DOI: 10.1080/10985549.2023.2171695

Lisa M Jorgenson, Lindsey Knight, Ray E Widner, Elizabeth A Rucks

{"title":"Eukaryotic Clathrin Adapter Protein and Mediator of Cholesterol Homeostasis, PICALM, Affects Trafficking to the Chlamydial Inclusion.","authors":"Lisa M Jorgenson, Lindsey Knight, Ray E Widner, Elizabeth A Rucks","doi":"10.1080/10985549.2023.2171695","DOIUrl":"10.1080/10985549.2023.2171695","url":null,"abstract":"The obligate intracellular pathogen Chlamydia trachomatis has unique metabolic requirements as it proceeds through its biphasic developmental cycle from within the inclusion within the host cell. In our previous study, we identified a host protein, PICALM, which localizes to the chlamydial inclusion. PICALM functions in many host pathways including the recycling of receptors, specific SNARE proteins, and molecules like transferrin, and maintaining cholesterol homeostasis. Hence, we hypothesized that PICALM functions to maintain the cholesterol content and to moderate trafficking from the endosomal recycling pathway to the inclusion, which controls chlamydial access to this pathway. In uninfected cells, siRNA knockdown of PICALM resulted in increased cholesterol within the Golgi and transferrin receptor (TfR) positive vesicles (recycling endosomes). PICALM knockdown in cells infected with C. trachomatis resulted in increased levels of Golgi-derived lipid and protein, TfR, transferrin, and Rab11-FIP1 localized to inclusions and a decrease of Golgi fragmentation at and Rab11 trafficking to the inclusion. Interestingly, chlamydial infection alone also increases cholesterol in TfR and Rab11-associated vesicles, and PICALM knockdown reverses this effect. Our data suggest that PICALM functions to balance or limit chlamydial access to multiple subcellular trafficking pathways to maintain the health of the host cell during chlamydial infection.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"1-13"},"PeriodicalIF":5.3,"publicationDate":"2023-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9980547/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10826428","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

Incomplete Elongation of Ultra-long-chain Polyunsaturated Acyl-CoAs by the Fatty Acid Elongase ELOVL4 in Spinocerebellar Ataxia Type 34. 脊髓小脑共济失调 34 型中脂肪酸延伸酶 ELOVL4 对超长链多不饱和酰基-CoAs 的不完全延伸。

IF 5.3 2区生物学

Molecular and Cellular Biology Pub Date : 2023-02-07 DOI: 10.1080/10985549.2023.2169563

Yuka Tamura, Takayuki Sassa, Takumi Nishizawa, Akio Kihara

{"title":"Incomplete Elongation of Ultra-long-chain Polyunsaturated Acyl-CoAs by the Fatty Acid Elongase ELOVL4 in Spinocerebellar Ataxia Type 34.","authors":"Yuka Tamura, Takayuki Sassa, Takumi Nishizawa, Akio Kihara","doi":"10.1080/10985549.2023.2169563","DOIUrl":"10.1080/10985549.2023.2169563","url":null,"abstract":"Spinocerebellar ataxias (SCAs) are autosomal dominant diseases characterized by cerebellar atrophy and ataxia. The SCA subtype SCA34 is caused by specific mutations in the gene ELOVL4, which encodes a fatty acid (FA) elongase that synthesizes ultra-long-chain (ULC; ≥C26) FAs. However, the pathogenesis and molecular mechanism that confers dominant inheritance remains unknown. Here, a cell-based assay demonstrated that each of the five known SCA34 mutants produced shorter ULC polyunsaturated FA-containing phosphatidylcholines (ULC-PCs) than wild-type protein, in the following order of severity: Q180P and T233M > W246G > I171T and L168F. Next, we generated knock-in mouse embryonic stem cells that contained heterozygous Q180P, heterozygous W246G, or homozygous W246G mutations. Neuronal differentiation-dependent production of ULC-PCs was reduced in heterozygous Q180P and homozygous W246G cells relative to control cells, and we observed shortening of the FA moiety in all mutant cells. This FA shortening was consistent with our prediction that amino acid residues substituted by SCA34 mutations are located in the transmembrane helices that interact with the ω-end region of the FA moiety of the substrate acyl-CoA. Hence, reduced levels and shortening of ULC-PCs in neurons may cause SCA34, and incomplete elongation of ULC polyunsaturated acyl-CoAs by mutated ELOVL4 may induce dominant inheritance.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"1-17"},"PeriodicalIF":5.3,"publicationDate":"2023-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9980445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9371312","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

Sumoylation is Largely Dispensable for Normal Growth but Facilitates Heat Tolerance in Yeast. sumo化在酵母的正常生长中是必不可少的，但它促进了酵母的耐热性。

IF 5.3 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 DOI: 10.1080/10985549.2023.2166320

Marjan Moallem, Akhi Akhter, Giovanni L Burke, John Babu, Benjamin G Bergey, J Bryan McNeil, Mohammad S Baig, Emanuel Rosonina

{"title":"Sumoylation is Largely Dispensable for Normal Growth but Facilitates Heat Tolerance in Yeast.","authors":"Marjan Moallem, Akhi Akhter, Giovanni L Burke, John Babu, Benjamin G Bergey, J Bryan McNeil, Mohammad S Baig, Emanuel Rosonina","doi":"10.1080/10985549.2023.2166320","DOIUrl":"https://doi.org/10.1080/10985549.2023.2166320","url":null,"abstract":"Numerous proteins are sumoylated in normally growing yeast and SUMO conjugation levels rise upon exposure to several stress conditions. We observe high levels of sumoylation also during early exponential growth and when nutrient-rich medium is used. However, we find that reduced sumoylation (∼75% less than normal) is remarkably well-tolerated, with no apparent growth defects under nonstress conditions or under osmotic, oxidative, or ethanol stresses. In contrast, strains with reduced activity of Ubc9, the sole SUMO conjugase, are temperature-sensitive, implicating sumoylation in the heat stress response, specifically. Aligned with this, a mild heat shock triggers increased sumoylation which requires functional levels of Ubc9, but likely also depends on decreased desumoylation, since heat shock reduces protein levels of Ulp1, the major SUMO protease. Furthermore, we find that a ubc9 mutant strain with only ∼5% of normal sumoylation levels shows a modest growth defect, has abnormal genomic distribution of RNA polymerase II (RNAPII), and displays a greatly expanded redistribution of RNAPII after heat shock. Together, our data implies that SUMO conjugations are largely dispensable under normal conditions, but a threshold level of Ubc9 activity is needed to maintain transcriptional control and to modulate the redistribution of RNAPII and promote survival when temperatures rise.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":"43 1","pages":"64-84"},"PeriodicalIF":5.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/5a/58/TMCB_43_2166320.PMC9936996.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9176401","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: 1

Exosome-transmitted circIFNGR2 Modulates Ovarian Cancer Metastasis via miR-378/ST5 Axis. 外泌体传递的circIFNGR2通过miR-378/ST5轴调节卵巢癌转移

IF 5.3 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 Epub Date: 2023-01-26 DOI: 10.1080/10985549.2022.2160605

Xiaoping Chen, Xinping Ren, Jiaoting E, Yaqi Zhou, Rongfang Bian

{"title":"Exosome-transmitted circIFNGR2 Modulates Ovarian Cancer Metastasis via miR-378/ST5 Axis.","authors":"Xiaoping Chen, Xinping Ren, Jiaoting E, Yaqi Zhou, Rongfang Bian","doi":"10.1080/10985549.2022.2160605","DOIUrl":"10.1080/10985549.2022.2160605","url":null,"abstract":"Cancer-associated fibroblasts (CAFs)-derived exosomes have emerged as a key driver of ovarian cancer (OVCA) tumor progression. The mechanisms behind the specific circular RNA (circRNA) activity encapsulated by CAF-generated exosomes (CAF-exo) requires to be elucidated. Herein, this study selected specific circRNA (hsa_circIFNGR2) molecules and aimed to clarify novel function of CAF-derived exosomal circIFNGR2 on growth, and metastasis of OVCA cells. In this study, we clarified that the exosomes of CAFs originating from human ovarian cancer hindered tumor cell proliferation, metastasis and EMT in vitro. Interestingly, CAFs directly transferred exosomes into OVCA cells to enrich intracellular circIFNGR2 levels. Biologically, activation of exosomal circIFNGR2 blocked cell proliferation, metastasis and EMT. Mechanistically, enhanced circIFNGR2 activated the miR-378/ST5 axis and directly inhibited the malignant evolution of tumor cells. Furthermore, rescue experiments evidenced that circIFNGR2 and ST5 were two essential participants in OVCA, concretely manifested in the co-culture of OVCA cells with exosomes that reversed the effects of intracellular circIFNGR2 and ST5 depletion. Finally, we observed that CAF-exo treatment hindered tumor growth and increased the size and number of metastatic nodules in mice. Our study revealed a previously unknown regulatory pathway whereby CAFs-derived exosomes delivered circIFNGR2 and inhibited the malignant progression of OVCA by circIFNGR2/miR-378/ST5 axis.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":"43 1","pages":"22-42"},"PeriodicalIF":5.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9937009/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9120083","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

CircTTLL13 Promotes TMZ Resistance in Glioma via Modulating OLR1-Mediated Activation of the Wnt/β-Catenin Pathway. CircTTLL13 通过调节 OLR1 介导的 Wnt/β-Catenin 通路激活促进胶质瘤的 TMZ 抗性

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 Epub Date: 2023-07-10 DOI: 10.1080/10985549.2023.2210032

Jun Li, Junfeng Ma, Shan Huang, Jun Li, Liang Zhou, Jiahua Sun, Lin Chen

{"title":"CircTTLL13 Promotes TMZ Resistance in Glioma via Modulating OLR1-Mediated Activation of the Wnt/β-Catenin Pathway.","authors":"Jun Li, Junfeng Ma, Shan Huang, Jun Li, Liang Zhou, Jiahua Sun, Lin Chen","doi":"10.1080/10985549.2023.2210032","DOIUrl":"10.1080/10985549.2023.2210032","url":null,"abstract":"Glioma, originating from neuroglial progenitor cells, is a type of intrinsic brain tumor with poor prognosis. temozolomide (TMZ) is the first-line chemotherapeutic agent for glioma. Exploring the mechanisms of circTTLL13 underlying TMZ resistance in glioma is of great significance to improve glioma treatment. Bioinformatics was adopted to identify target genes. The circular structure of circTTLL13 and its high expression in glioma cells were disclosed by quantitative real time-PCR (qRT-PCR) and PCR-agarose gel electrophoresis. Functional experiments proved that oxidized LDL receptor 1 (OLR1) promotes TMZ resistance of glioma cells. CircTTLL13 enhances TMZ resistance of glioma cells via modulating OLR1. Luciferase reporter, RNA-binding protein immunoprecipitation (RIP), RNA pulldown, mRNA stability, N6-methyladenosine (m6A) dot blot and RNA total m6A quantification assays were implemented, indicating that circTTLL13 stabilizes OLR1 mRNA via recruiting YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) and promotes m6A methylation of OLR1 pre-mRNA through recruiting methyltransferase-like 3 (METTL3). TOP/FOP-flash reporter assay and western blot verified that circTTLL13 activates Wnt/β-catenin signaling pathway by regulating OLR1. CircTTLL13 promotes TMZ resistance in glioma through regulating OLR1-mediated Wnt/β-catenin pathway activation. This study offers an insight into the efficacy improvement of TMZ for glioma treatment.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":"43 7","pages":"354-369"},"PeriodicalIF":3.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10348032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9809223","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

EPRS1 Controls the TGF-β Signaling Pathway via Interaction with TβRI in Hepatic Stellate Cell. EPRS1通过与TβRI相互作用调控肝星状细胞TGF-β信号通路。

IF 5.3 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 DOI: 10.1080/10985549.2023.2205344

Ina Yoon, Ji Ae Song, Ji Hun Suh, Sulhee Kim, Jonghyeon Son, Jong Hyun Kim, Song Yee Jang, Kwang Yeon Hwang, Myung Hee Kim, Sunghoon Kim

{"title":"EPRS1 Controls the TGF-β Signaling Pathway via Interaction with TβRI in Hepatic Stellate Cell.","authors":"Ina Yoon, Ji Ae Song, Ji Hun Suh, Sulhee Kim, Jonghyeon Son, Jong Hyun Kim, Song Yee Jang, Kwang Yeon Hwang, Myung Hee Kim, Sunghoon Kim","doi":"10.1080/10985549.2023.2205344","DOIUrl":"https://doi.org/10.1080/10985549.2023.2205344","url":null,"abstract":"Glutamyl-prolyl-tRNA synthetase 1 (EPRS1) is known to associated with fibrosis through its catalytic activity to produce prolyl-tRNA. Although its catalytic inhibitor halofuginone (HF) has been known to inhibit the TGF-β pathway as well as to reduce prolyl-tRNA production for the control of fibrosis, the underlying mechanism how EPRS1 regulates the TGF-β pathway was not fully understood. Here, we show a noncatalytic function of EPRS1 in controlling the TGF-β pathway and hepatic stellate cell activation via its interaction with TGF-β receptor I (TβRI). Upon stimulation with TGF-β, EPRS1 is phosphorylated by TGF-β-activated kinase 1 (TAK1), leading to its dissociation from the multi-tRNA synthetase complex and subsequent binding with TβRI. This interaction increases the association of TβRI with SMAD2/3 while decreases that of TβRI with SMAD7. Accordingly, EPRS1 stabilizes TβRI by preventing the ubiquitin-mediated degradation of TβRI. HF disrupts the interaction between EPRS1 and TβRI, and reduces TβRI protein levels, leading to inhibition of the TGF-β pathway. In conclusion, this work suggests the novel function of EPRS1 involved in the development of fibrosis by regulating the TGF-β pathway and the antifibrotic effects of HF by controlling both of EPRS1 functions.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":"43 5","pages":"223-240"},"PeriodicalIF":5.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/83/de/TMCB_43_2205344.PMC10184599.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9828104","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: 1

microRNA-130b May Induce Cerebral Vasospasm after Subarachnoid Hemorrhage via Modulating Kruppel-like Factor 4. microRNA-130b可能通过调节kruppel样因子4诱导蛛网膜下腔出血后脑血管痉挛。

IF 5.3 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 DOI: 10.1080/10985549.2023.2210030

Zewei Huang, Jiliang Hu, Jiongfu Xu, Hao Wang, Limeng Dai

{"title":"microRNA-130b May Induce Cerebral Vasospasm after Subarachnoid Hemorrhage via Modulating Kruppel-like Factor 4.","authors":"Zewei Huang, Jiliang Hu, Jiongfu Xu, Hao Wang, Limeng Dai","doi":"10.1080/10985549.2023.2210030","DOIUrl":"https://doi.org/10.1080/10985549.2023.2210030","url":null,"abstract":"Recently, the diverse functions of microRNAs (miRNAs) in brain diseases have been demonstrated. We intended to uncover the functional role of microRNA-130b (miR-130b) in cerebral vasospasm (CVS) following subarachnoid hemorrhage (SAH). SAH was induced by injecting the autologous blood into the cisterna magna of Sprague Dawley rats. The cerebral vascular smooth muscle cells (cVSMCs) were extracted for in vitro experimentation. In vitro and in vivo assays were implemented with transfection of miR-130b mimic/inhibitor, sh-Kruppel-like factor 4 (KLF4), oe-KLF4 plasmids or p38/MAPK signaling pathway agonist (anisomycin), respectively, to elaborate the role of miR-130b in CVS following SAH. Elevated miR-130b and reduced KLF4 were found in SAH patients and rat models of SAH. KLF4 was the target gene of miR-130b. miR-130b promoted the proliferation and migration of cVSMCs through the Inhibition of KLF4. Besides, KLF4 inhibited the proliferation and migration of cVSMCs through blockage of the p38/MAPK pathway. Furthermore, in vivo assay confirmed the inhibitory effect of decreased miR-130b in CVS following SAH. In conclusion, miR-130b may activate the p38/MAPK signaling pathway through targeted inhibition of KLF4, thereby contributing to some extent to the development of cerebral vasospasm after SAH.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":"43 7","pages":"301-316"},"PeriodicalIF":5.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/98/cc/TMCB_43_2210030.PMC10348024.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9835351","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

Receptor Recycling by Retromer. Retromer 的受体再循环。

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 Epub Date: 2023-06-23 DOI: 10.1080/10985549.2023.2222053

Julian M Carosi, Donna Denton, Sharad Kumar, Timothy J Sargeant

{"title":"Receptor Recycling by Retromer.","authors":"Julian M Carosi, Donna Denton, Sharad Kumar, Timothy J Sargeant","doi":"10.1080/10985549.2023.2222053","DOIUrl":"10.1080/10985549.2023.2222053","url":null,"abstract":"The highly conserved retromer complex controls the fate of hundreds of receptors that pass through the endolysosomal system and is a central regulatory node for diverse metabolic programs. More than 20 years ago, retromer was discovered as an essential regulator of endosome-to-Golgi transport in yeast; since then, significant progress has been made to characterize how metazoan retromer components assemble to enable its engagement with endosomal membranes, where it sorts cargo receptors from endosomes to the trans-Golgi network or plasma membrane through recognition of sorting motifs in their cytoplasmic tails. In this review, we examine retromer regulation by exploring its assembled structure with an emphasis on how a range of adaptor proteins shape the process of receptor trafficking. Specifically, we focus on how retromer is recruited to endosomes, selects cargoes, and generates tubulovesicular carriers that deliver cargoes to target membranes. We also examine how cells adapt to distinct metabolic states by coordinating retromer expression and function. We contrast similarities and differences between retromer and its related complexes: retriever and commander/CCC, as well as their interplay in receptor trafficking. We elucidate how loss of retromer regulation is central to the pathology of various neurogenerative and metabolic diseases, as well as microbial infections, and highlight both opportunities and cautions for therapeutics that target retromer. Finally, with a focus on understanding the mechanisms that govern retromer regulation, we outline new directions for the field moving forward.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":"43 7","pages":"317-334"},"PeriodicalIF":3.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10348044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9799013","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