Molecular and Cellular Biology最新文献_第9页

Dematin Regulates Calcium Mobilization, Thrombosis, and Early Akt Activation in Platelets. Dematin 可调节血小板中的钙动员、血栓形成和早期 Akt 激活。

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 Epub Date: 2023-05-22 DOI: 10.1080/10985549.2023.2210033

Daniel I Fritz, Yiwen Ding, Glenn Merrill-Skoloff, Robert Flaumenhaft, Toshihiko Hanada, Athar H Chishti

{"title":"Dematin Regulates Calcium Mobilization, Thrombosis, and Early Akt Activation in Platelets.","authors":"Daniel I Fritz, Yiwen Ding, Glenn Merrill-Skoloff, Robert Flaumenhaft, Toshihiko Hanada, Athar H Chishti","doi":"10.1080/10985549.2023.2210033","DOIUrl":"10.1080/10985549.2023.2210033","url":null,"abstract":"The complex intrinsic and extrinsic pathways contributing to platelet activation profoundly impact hemostasis and thrombosis. Detailed cellular mechanisms that regulate calcium mobilization, Akt activation, and integrin signaling in platelets remain incompletely understood. Dematin is a broadly expressed actin binding and bundling cytoskeletal adaptor protein regulated by phosphorylation via cAMP-dependent protein kinase. Here, we report the development of a conditional mouse model specifically lacking dematin in platelets. Using the new mouse model termed PDKO, we provide direct evidence that dematin is a major regulator of calcium mobilization, and its genetic deletion inhibits the early phase of Akt activation in response to collagen and thrombin agonists in platelets. The aberrant platelet shape change, clot retraction, and in vivo thrombosis observed in PDKO mice will enable future characterization of dematin-mediated integrin activation mechanisms in thrombogenic as well as nonvascular pathologies.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":"43 6","pages":"283-299"},"PeriodicalIF":3.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10251785/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9667900","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 Sequential Recruitments of Rab-GTPase Ypt1p and the NNS Complex onto pre-HAC1 mRNA Promote Its Nuclear Degradation in Baker's Yeast. Rab GTPase Ypt1p和NNS复合物在前HAC1 mRNA上的顺序募集促进其在贝克酵母中的核降解。

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 Epub Date: 2023-08-02 DOI: 10.1080/10985549.2023.2227016

Sunirmal Paira, Anish Chakraborty, Biswadip Das

{"title":"The Sequential Recruitments of Rab-GTPase Ypt1p and the NNS Complex onto pre-HAC1 mRNA Promote Its Nuclear Degradation in Baker's Yeast.","authors":"Sunirmal Paira, Anish Chakraborty, Biswadip Das","doi":"10.1080/10985549.2023.2227016","DOIUrl":"10.1080/10985549.2023.2227016","url":null,"abstract":"Induction of unfolded protein response involves activation of transcription factor Hac1p that is encoded by HAC1 pre-mRNA harboring an intron and a bipartite element (BE), which is subjected to nuclear mRNA decay by the nuclear exosome/Cbc1p-Tif4631p-dependent Exosome Targeting (CTEXT) complex. Using a combination of genetic and biochemical approaches, we demonstrate that a Rab-GTPase Ypt1p controls unfolded protein response signaling dynamics. This regulation relies on the nuclear localization of a small fraction of the cellular Ypt1p pool in the absence of endoplasmic reticulum (ER)-stress causing a strong association of the nuclear Ypt1p with pre-HAC1 mRNA that eventually promotes sequential recruitments of NNS, CTEXT, and the nuclear exosome onto this pre-mRNA. Recruitment of these decay factors onto pre-HAC1 mRNA is accompanied by its rapid nuclear decay that produces a precursor RNA pool lacking functional BE thereby causing its inefficient targeting to Ire1p foci leading to their diminished splicing and translation. ER stress triggers rapid relocalization of the nuclear pool of Ypt1p to the cytoplasm leading to its dissociation from pre-HAC1 mRNA thereby causing decreased recruitment of these decay factors to precursor HAC1 RNA leading to its diminished degradation. Reduced decay results in an increased abundance of pre-HAC1 mRNA with intact functional BE leading to its enhanced recruitment to Ire1p foci.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":"43 8","pages":"371-400"},"PeriodicalIF":3.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10448977/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10102467","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

Implications of Translesion DNA Synthesis Polymerases on Genomic Stability and Human Health. 翻译DNA合成聚合酶对基因组稳定性和人类健康的影响。

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 Epub Date: 2023-07-13 DOI: 10.1080/10985549.2023.2224199

Jegadheeswari Venkadakrishnan, Ganesh Lahane, Arti Dhar, Wei Xiao, Krishna Moorthi Bhat, Tej K Pandita, Audesh Bhat

{"title":"Implications of Translesion DNA Synthesis Polymerases on Genomic Stability and Human Health.","authors":"Jegadheeswari Venkadakrishnan, Ganesh Lahane, Arti Dhar, Wei Xiao, Krishna Moorthi Bhat, Tej K Pandita, Audesh Bhat","doi":"10.1080/10985549.2023.2224199","DOIUrl":"10.1080/10985549.2023.2224199","url":null,"abstract":"Replication fork arrest-induced DNA double strand breaks (DSBs) caused by lesions are effectively suppressed in cells due to the presence of a specialized mechanism, commonly referred to as DNA damage tolerance (DDT). In eukaryotic cells, DDT is facilitated through translesion DNA synthesis (TLS) carried out by a set of DNA polymerases known as TLS polymerases. Another parallel mechanism, referred to as homology-directed DDT, is error-free and involves either template switching or fork reversal. The significance of the DDT pathway is well established. Several diseases have been attributed to defects in the TLS pathway, caused either by mutations in the TLS polymerase genes or dysregulation. In the event of a replication fork encountering a DNA lesion, cells switch from high-fidelity replicative polymerases to low-fidelity TLS polymerases, which are associated with genomic instability linked with several human diseases including, cancer. The role of TLS polymerases in chemoresistance has been recognized in recent years. In addition to their roles in the DDT pathway, understanding noncanonical functions of TLS polymerases is also a key to unraveling their importance in maintaining genomic stability. Here we summarize the current understanding of TLS pathway in DDT and its implication for human health.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":"43 8","pages":"401-425"},"PeriodicalIF":3.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10448981/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10425833","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

Distinct Interaction Modes for the Eukaryotic RNA Polymerase Alpha-like Subunits. 真核生物 RNA 聚合酶 Alpha 类亚基的不同相互作用模式

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 Epub Date: 2023-05-24 DOI: 10.1080/10985549.2023.2210023

Alana E Belkevich, Haleigh G Pascual, Aula M Fakhouri, David G Ball, Bruce A Knutson

{"title":"Distinct Interaction Modes for the Eukaryotic RNA Polymerase Alpha-like Subunits.","authors":"Alana E Belkevich, Haleigh G Pascual, Aula M Fakhouri, David G Ball, Bruce A Knutson","doi":"10.1080/10985549.2023.2210023","DOIUrl":"10.1080/10985549.2023.2210023","url":null,"abstract":"Eukaryotic DNA-dependent RNA polymerases (Pols I-III) encode two distinct alpha-like heterodimers where one is shared between Pols I and III, and the other is unique to Pol II. Human alpha-like subunit mutations are associated with several diseases including Treacher Collins Syndrome (TCS), 4H leukodystrophy, and primary ovarian sufficiency. Yeast is commonly used to model human disease mutations, yet it remains unclear whether the alpha-like subunit interactions are functionally similar between yeast and human homologs. To examine this, we mutated several regions of the yeast and human small alpha-like subunits and used biochemical and genetic assays to establish the regions and residues required for heterodimerization with their corresponding large alpha-like subunits. Here we show that different regions of the small alpha-like subunits serve differential roles in heterodimerization, in a polymerase- and species-specific manner. We found that the small human alpha-like subunits are more sensitive to mutations, including a \"humanized\" yeast that we used to characterize the molecular consequence of the TCS-causingPOLR1D G52E mutation. These findings help explain why some alpha subunit associated disease mutations have little to no effect when made in their yeast orthologs and offer a better yeast model to assess the molecular basis of POLR1D associated disease mutations.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":"43 6","pages":"269-282"},"PeriodicalIF":3.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10251799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9605115","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

Chaperone-Dependent Degradation of Cdc42 Promotes Cell Polarity and Shields the Protein from Aggregation. 蛋白伴侣依赖性降解 Cdc42 可促进细胞极性并防止蛋白质聚集。

IF 5.3 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 Epub Date: 2023-04-28 DOI: 10.1080/10985549.2023.2198171

Beatriz González, Martí Aldea, Paul J Cullen

{"title":"Chaperone-Dependent Degradation of Cdc42 Promotes Cell Polarity and Shields the Protein from Aggregation.","authors":"Beatriz González, Martí Aldea, Paul J Cullen","doi":"10.1080/10985549.2023.2198171","DOIUrl":"10.1080/10985549.2023.2198171","url":null,"abstract":"Rho GTPases are global regulators of cell polarity and signaling. By exploring the turnover regulation of the yeast Rho GTPase Cdc42p, we identified new regulatory features surrounding the stability of the protein. We specifically show that Cdc42p is degraded at 37 °C by chaperones through lysine residues located in the C-terminus of the protein. Cdc42p turnover at 37 °C occurred by the 26S proteasome in an ESCRT-dependent manner in the lysosome/vacuole. By analyzing versions of Cdc42p that were defective for turnover, we show that turnover at 37 °C promoted cell polarity but was defective for sensitivity to mating pheromone, presumably mediated through a Cdc42p-dependent MAP kinase pathway. We also identified one residue (K16) in the P-loop of the protein that was critical for Cdc42p stability. Accumulation of Cdc42pK16R in some contexts led to the formation of protein aggregates, which were enriched in aging mother cells and cells undergoing proteostatic stress. Our study uncovers new aspects of protein turnover regulation of a Rho-type GTPase that may extend to other systems. Moreover, residues identified here that mediate Cdc42p turnover correlate with several human diseases, which may suggest that turnover regulation of Cdc42p is important to aspects of human health.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":"43 5","pages":"200-222"},"PeriodicalIF":5.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10184603/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9510794","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

Shared Gene Targets of the ATF4 and p53 Transcriptional Networks. ATF4和p53转录网络的共享基因靶点。

IF 5.3 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 Epub Date: 2023-08-02 DOI: 10.1080/10985549.2023.2229225

Gabriele Baniulyte, Serene A Durham, Lauren E Merchant, Morgan A Sammons

{"title":"Shared Gene Targets of the ATF4 and p53 Transcriptional Networks.","authors":"Gabriele Baniulyte, Serene A Durham, Lauren E Merchant, Morgan A Sammons","doi":"10.1080/10985549.2023.2229225","DOIUrl":"10.1080/10985549.2023.2229225","url":null,"abstract":"The master tumor suppressor p53 regulates multiple cell fate decisions, such as cell cycle arrest and apoptosis, via transcriptional control of a broad gene network. Dysfunction in the p53 network is common in cancer, often through mutations that inactivate p53 or other members of the pathway. Induction of tumor-specific cell death by restoration of p53 activity without off-target effects has gained significant interest in the field. In this study, we explore the gene regulatory mechanisms underlying a putative anticancer strategy involving stimulation of the p53-independent integrated stress response (ISR). Our data demonstrate the p53 and ISR pathways converge to independently regulate common metabolic and proapoptotic genes. We investigated the architecture of multiple gene regulatory elements bound by p53 and the ISR effector ATF4 controlling this shared regulation. We identified additional key transcription factors that control basal and stress-induced regulation of these shared p53 and ATF4 target genes. Thus, our results provide significant new molecular and genetic insight into gene regulatory networks and transcription factors that are the target of numerous antitumor therapies.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":"43 8","pages":"426-449"},"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/ec/fa/TMCB_43_2229225.PMC10448979.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10426326","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

Persistent Acetylation of Histone H3 Lysine 56 Compromises the Activity of DNA Replication Origins. 组蛋白H3赖氨酸56的持续乙酰化损害DNA复制起源的活性。

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 Epub Date: 2023-11-17 DOI: 10.1080/10985549.2023.2259739

Roch Tremblay, Yosra Mehrjoo, Oumaima Ahmed, Antoine Simoneau, Mary E McQuaid, El Bachir Affar, Corey Nislow, Guri Giaever, Hugo Wurtele

{"title":"Persistent Acetylation of Histone H3 Lysine 56 Compromises the Activity of DNA Replication Origins.","authors":"Roch Tremblay, Yosra Mehrjoo, Oumaima Ahmed, Antoine Simoneau, Mary E McQuaid, El Bachir Affar, Corey Nislow, Guri Giaever, Hugo Wurtele","doi":"10.1080/10985549.2023.2259739","DOIUrl":"10.1080/10985549.2023.2259739","url":null,"abstract":"In Saccharomyces cerevisiae, newly synthesized histones H3 are acetylated on lysine 56 (H3 K56ac) by the Rtt109 acetyltransferase prior to their deposition on nascent DNA behind replication forks. Two deacetylases of the sirtuin family, Hst3 and Hst4, remove H3 K56ac from chromatin after S phase. hst3Δ hst4Δ cells present constitutive H3 K56ac, which sensitizes cells to replicative stress via unclear mechanisms. A chemogenomic screen revealed that DBF4 heterozygosity sensitizes cells to NAM-induced inhibition of sirtuins. DBF4 and CDC7 encode subunits of the Dbf4-dependent kinase (DDK), which activates origins of DNA replication during S phase. We show that (i) cells harboring the dbf4-1 or cdc7-4 hypomorphic alleles are sensitized to NAM, and that (ii) the sirtuins Sir2, Hst1, Hst3, and Hst4 promote DNA replication in cdc7-4 cells. We further demonstrate that Rif1, an inhibitor of DDK-dependent activation of origins, causes DNA damage and replication defects in NAM-treated cells and hst3Δ hst4Δ mutants. cdc7-4 hst3Δ hst4Δ cells are shown to display delayed initiation of DNA replication, which is not due to intra-S checkpoint activation but requires Rtt109-dependent H3 K56ac. Our results suggest that constitutive H3 K56ac sensitizes cells to replicative stress in part by negatively influencing the activation of origins of DNA replication.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"566-595"},"PeriodicalIF":3.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10791153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41127303","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

Functional Consequences of Shifting Transcript Boundaries in Glucose Starvation. 葡萄糖饥饿中转录边界转移的功能后果。

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 Epub Date: 2023-11-17 DOI: 10.1080/10985549.2023.2270406

Lan Anh Catherine Nguyen, Masaru Mori, Yuji Yasuda, Josephine Galipon

{"title":"Functional Consequences of Shifting Transcript Boundaries in Glucose Starvation.","authors":"Lan Anh Catherine Nguyen, Masaru Mori, Yuji Yasuda, Josephine Galipon","doi":"10.1080/10985549.2023.2270406","DOIUrl":"10.1080/10985549.2023.2270406","url":null,"abstract":"Glucose is a major source of carbon and essential for the survival of many organisms, ranging from yeast to human. A sudden 60-fold reduction of glucose in exponentially growing fission yeast induces transcriptome-wide changes in gene expression. This regulation is multilayered, and the boundaries of transcripts are known to vary, with functional consequences at the protein level. By combining direct RNA sequencing with 5'-CAGE and short-read sequencing, we accurately defined the 5'- and 3'-ends of transcripts that are both poly(A) tailed and 5'-capped in glucose starvation, followed by proteome analysis. Our results confirm previous experimentally validated loci with alternative isoforms and reveal several transcriptome-wide patterns. First, we show that sense-antisense gene pairs are more strongly anticorrelated when a time lag is taken into account. Second, we show that the glucose starvation response initially elicits a shortening of 3'-UTRs and poly(A) tails, followed by a shortening of the 5'-UTRs at later time points. These result in domain gains and losses in proteins involved in the stress response. Finally, the relatively poor overlap both between differentially expressed genes (DEGs), differential transcript usage events (DTUs), and differentially detected proteins (DDPs) highlight the need for further study on post-transcriptional regulation mechanisms in glucose starvation.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"611-628"},"PeriodicalIF":3.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10761120/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71483578","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

Genetic and Pharmacological Modulation of Cellular Proteostasis Leads to Partial Functional Rescue of Homocystinuria-Causing Cystathionine-Beta Synthase Variants. 通过基因和药物调节细胞蛋白稳态可部分修复高胱氨酸尿症致病胱硫醚-β合成酶变异体的功能。

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 Epub Date: 2023-12-20 DOI: 10.1080/10985549.2023.2284147

Renata Collard, Tomas Majtan

{"title":"Genetic and Pharmacological Modulation of Cellular Proteostasis Leads to Partial Functional Rescue of Homocystinuria-Causing Cystathionine-Beta Synthase Variants.","authors":"Renata Collard, Tomas Majtan","doi":"10.1080/10985549.2023.2284147","DOIUrl":"10.1080/10985549.2023.2284147","url":null,"abstract":"Homocystinuria (HCU), an inherited metabolic disorder caused by lack of cystathionine beta-synthase (CBS) activity, is chiefly caused by misfolding of single amino acid residue missense pathogenic variants. Previous studies showed that chemical, pharmacological chaperones or proteasome inhibitors could rescue function of multiple pathogenic CBS variants; however, the underlying mechanisms remain poorly understood. Using Chinese hamster DON fibroblasts devoid of CBS and stably overexpressing human WT or mutant CBS, we showed that expression of pathogenic CBS variant mostly dysregulates gene expression of small heat shock proteins HSPB3 and HSPB8 and members of HSP40 family. Endoplasmic reticulum stress sensor BiP was found upregulated with CBS I278T variant associated with proteasomes suggesting proteotoxic stress and degradation of misfolded CBS. Co-expression of the main effector HSP70 or master regulator HSF1 rescued steady-state levels of CBS I278T and R125Q variants with partial functional rescue of the latter. Pharmacological proteostasis modulators partially rescued expression and activity of CBS R125Q likely due to reduced proteotoxic stress as indicated by decreased BiP levels and promotion of refolding as indicated by induction of HSP70. In conclusion, targeted manipulation of cellular proteostasis may represent a viable therapeutic approach for the permissive pathogenic CBS variants causing HCU.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"664-674"},"PeriodicalIF":3.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10761163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138487995","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

Correction. 更正。

IF 5.3 2区生物学

Molecular and Cellular Biology Pub Date : 2023-01-01 Epub Date: 2023-12-20 DOI: 10.1080/10985549.2023.2289812

引用次数: 0