Journal of cellular signaling最新文献

PAX-Interacting Protein 1 (PTIP) Promotes Apoptosis. pax相互作用蛋白1 （PTIP）促进细胞凋亡。

Journal of cellular signaling Pub Date : 2025-01-01 DOI: 10.33696/signaling.6.142

Ching-Jung Huang, Hyein Cho, Chuan Li, Kangsan Kim, Danyang Yu, Daechan Park, Y Jessie Zhang, Haley O Tucker

引用次数: 0

CRABP1 Signalosomes in Cellular Stress Response and Health Maintenance. 细胞应激反应和健康维持中的CRABP1信号体。

Journal of cellular signaling Pub Date : 2025-01-01 DOI: 10.33696/signaling.6.141

Jennifer Nhieu, Fatimah Najjar, Li-Na Wei

引用次数: 0

Tumor Lipid Signaling Involved in Hyperoxidative Stress Response: Insights for Therapeutic Advances. 肿瘤脂质信号参与高氧化应激反应：治疗进展的见解。

Journal of cellular signaling Pub Date : 2025-01-01 DOI: 10.33696/Signaling.6.132

Mladen Korbelik, Albert W Girotti

{"title":"Tumor Lipid Signaling Involved in Hyperoxidative Stress Response: Insights for Therapeutic Advances.","authors":"Mladen Korbelik, Albert W Girotti","doi":"10.33696/Signaling.6.132","DOIUrl":"10.33696/Signaling.6.132","url":null,"abstract":"Most malignantly transformed cells are metabolically rewired to promote their survival and progression, even under conditions that would be unfavorable for normal counterparts. Arguably the most impactful metabolic transformation and recognized cancer hallmark is the reprogrammed lipid metabolism. Lipids are not only primary constituents of cell membranes but essential participants in fundamental cellular functions including cell signaling, protein regulation, energy provision, inflammation, and cell-cell interaction. Engagement of lipids in critical physiological functions in cells is additionally accentuated upon malignant transformation. Pivotal roles of lipids as influential inter- and intracellular signaling molecules, particularly under conditions of hyper oxidative stress, are delineated. Elaborated in more detail are SCAP/SREBP pathway and sphingolipid signaling cascades due to their roles of principal signaling networks determining tumor therapy responses. In the concluding section, an overview is provided of the process of lipid peroxidation and its impact in cancer cells sustaining oxidative stress with the outline of cell signaling functions of primary and secondary lipid peroxidation products. Much remains to be learned about the consequences of the fact that the lipid peroxidation process can extend beyond the site of initiation owing to (either spontaneous or transfer protein-mediated) translocation of peroxy radical species disseminating their impact to other subcellular sites.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"6 2","pages":"39-47"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12129048/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144210343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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 Newly Characterized, Two BRCT Domain-Containing Isoform of PAX-Interacting Protein (PTIP) Generated via Frame Shift and Alternative Pre-mRNA Splicing. 通过帧移位和可选Pre-mRNA剪接产生的pax相互作用蛋白（PTIP）的两个新特征的BRCT结构域异构体

Journal of cellular signaling Pub Date : 2025-01-01 DOI: 10.33696/signaling.6.143

Ching-Jung Huang, Chuan Li, Danyang Yu, Hyein Cho, Kangsan Kim, Y Jessie Zhang, Daechan Park, Haley O Tucker

引用次数: 0

Microcystin: From Blooms to Brain Toxicity. 微囊藻毒素：从大量繁殖到脑毒性。

Journal of cellular signaling Pub Date : 2025-01-01 DOI: 10.33696/Signaling.6.131

Ethan Hedrick, Aryaman Tiwari, Suryakant Niture, Qing Cheng, Deepak Kumar, Somnath Mukhopadhyay

{"title":"Microcystin: From Blooms to Brain Toxicity.","authors":"Ethan Hedrick, Aryaman Tiwari, Suryakant Niture, Qing Cheng, Deepak Kumar, Somnath Mukhopadhyay","doi":"10.33696/Signaling.6.131","DOIUrl":"10.33696/Signaling.6.131","url":null,"abstract":"An increase in the temperature of lakes and ponds facilitates the over-growth of photosynthetic cyanobacteria that produce a class of toxins called cyanotoxins. The abundance of cyanobacteria poses a significant threat to drinking and irrigation water supplies, and therefore, cyanotoxins have become a major class of environmental pollutants. Microcystins, the most common cyanotoxins, are cyclic peptides produced by cyanobacteria through non-ribosomal peptide synthases, and currently, approximately 279 microcystins have been identified to date. Exposure to microcystins can cause liver and brain cytotoxicity, dermatologic, gastrointestinal, respiratory, and neurologic signs and symptoms, and affect human health. Notably, microcystin-leucine arginine can breach the blood-brain barrier by the transporter proteins, organic anion transporting polypeptides, leading to neuroinflammation, and changes in neurocircuitry resulting in behavioral alterations. In this review, we provide an update of the current literature on the detrimental effects of microcystins on the brain, focusing on their potential role in Alzheimer's and Parkinson's diseases. We discuss the current findings along with the cellular mechanisms involved and provide a brief narrative of the scope of future studies, especially to address the effects of microcystins along with genetic and other risk factors (like alcohol and other drugs) on neurodegenerative disease.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"6 1","pages":"29-38"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12176425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144327986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ubiquitination of Metabotropic Glutamate Receptors and Associated Synaptic Proteins In Vitro and In Vivo. 代谢性谷氨酸受体及相关突触蛋白的泛素化研究。

Journal of cellular signaling Pub Date : 2025-01-01 DOI: 10.33696/Signaling.6.145

Li-Min Mao, John Q Wang

{"title":"Ubiquitination of Metabotropic Glutamate Receptors and Associated Synaptic Proteins In Vitro and In Vivo.","authors":"Li-Min Mao, John Q Wang","doi":"10.33696/Signaling.6.145","DOIUrl":"10.33696/Signaling.6.145","url":null,"abstract":"Metabotropic glutamate (mGlu) receptors are a family of G protein-coupled receptors. These receptors are widely distributed in the brain and are critical for the modulation of synaptic transmission and plasticity. Emerging evidence shows that mGlu receptors themselves are subject to a dynamic posttranslational modification involving protein ubiquitination. Postsynaptic group I mGlu receptors (mGlu1/5) undergo constitutive ubiquitination at lysine sites on their intracellular domains in heterologous cells and neurons. In particular, ligand stimulation triggers rapid ubiquitination of group I receptors to confer a negative feedback regulation. Like mGlu1/5, presynaptic mGlu7 receptors are ubiquitinated by a specific E3 ubiquitin ligase. Robust ubiquitination is also seen in a number of existing synaptic proteins closely associated with mGlu activity, including Homer1a, the activity-regulated cytoskeleton-associated protein Arc/Arg3.1, and the protein interacting with C-kinase 1. Ubiquitination of mGlu receptors targets the receptors to degradation via the proteasome-dependent or -independent pathway or plays nondegradative roles in the regulation of distinct cellular processes such as endocytic trafficking, protein-protein interactions, and mGlu receptor signaling.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"6 4","pages":"170-177"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12991066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147476221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pathogenic Pathways and Therapeutic Strategies in Autosomal Dominant Polycystic Kidney Disease (ADPKD). 常染色体显性多囊肾病（ADPKD）的致病途径和治疗策略。

Journal of cellular signaling Pub Date : 2025-01-01 DOI: 10.33696/signaling.6.144

Kenley M Preval, Abigail O Smith, Gregory J Pazour

{"title":"Pathogenic Pathways and Therapeutic Strategies in Autosomal Dominant Polycystic Kidney Disease (ADPKD).","authors":"Kenley M Preval, Abigail O Smith, Gregory J Pazour","doi":"10.33696/signaling.6.144","DOIUrl":"https://doi.org/10.33696/signaling.6.144","url":null,"abstract":"Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disorder and a major cause of end-stage renal disease. The disorder is primarily caused by pathogenic variants in PKD1 or PKD2, which encode the ciliary proteins polycystin-1 and polycystin-2. Loss of polycystin function disrupts calcium and cAMP signaling within the primary cilium, altering epithelial proliferation and fluid secretion that drive cyst formation and progressive kidney enlargement. Atypical forms of ADPKD arise from variants in genes required for the production of polycystins or for ciliary assembly. Cyst growth depends on proliferative and secretory pathways involving Ca2+, cAMP, mTORC1, Src, and receptor tyrosine kinases, while chloride and water transport via CFTR, ANO1, and NKCC1 drive luminal expansion. The vasopressin V2 receptor antagonists tolvaptan remains the only approved therapy, but new approaches are under investigation. These include inhibitors of mTORC1, Src, and RTKs, agents that block chloride secretion, small molecules and microRNAs that restore or enhance polycystin expression, and emerging cyst-directed cytotoxic therapies. By targeting aberrant epithelial responses to disrupted polycystin function, therapeutic intervention can be developed to halt cyst initiation, expansion, and progression to renal failure.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"6 4","pages":"156-169"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12842028/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146094966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Signaling of Mitogenic and Metabolic Activities by Fibroblast Growth Factors. 成纤维细胞生长因子对有丝分裂和代谢活动的信号传导。

Journal of cellular signaling Pub Date : 2025-01-01 DOI: 10.33696/signaling.6.127

Patience Salvalina Okoto, Zeina Alraawi, Thallapuranam Krishnaswamy Suresh Kumar

引用次数: 0

Role of Exosomal MicroRNAs in Modulating the Response of Cancer Cells to Paclitaxel Treatment 外泌体微RNA在调节癌细胞对紫杉醇治疗反应中的作用

Journal of cellular signaling Pub Date : 2024-03-01 DOI: 10.33696/signaling.5.111

Lan Zhao, Cheng Lv, Hui Xie, Xiaoxu Ding

引用次数: 0

Phorbol-12-Myristate-13-Acetate (PMA) Reactivates Replication from HIV-1 Latency and Induces Jurkat Cell Death 光稳定剂-12-肉豆蔻酸-13-乙酸酯（PMA）可激活潜伏期的 HIV-1 复制并诱导 Jurkat 细胞死亡

Journal of cellular signaling Pub Date : 2024-03-01 DOI: 10.33696/signaling.5.110

Xue Wang, Jiangqin Zhao, Indira Hewlett

{"title":"Phorbol-12-Myristate-13-Acetate (PMA) Reactivates Replication from HIV-1 Latency and Induces Jurkat Cell Death","authors":"Xue Wang, Jiangqin Zhao, Indira Hewlett","doi":"10.33696/signaling.5.110","DOIUrl":"https://doi.org/10.33696/signaling.5.110","url":null,"abstract":"HIV-1 has the capability to establish latency during early infection in CD4+ cells, posing a significant challenge to the efforts aimed at curing HIV-1/AIDS. One extensively explored strategy to address this viral latency is the \"shock-and-kill\" approach. This involves reactivating viral replication using latency reversal agents (LRAs) to induce the death of infected cells. Regrettably, no LRAs with proven effectiveness have been identified thus far. In this study, we investigated the impact of Azidothymidine (AZT) treatment interruption and the administration of Phorbol-12-Myristate-13-Acetate (PMA), a PKC activator, as shock-and-kill approaches in vitro. We employed the susceptible Jurkat cell line and utilized a sensitive real-time PCR assay along with Western blotting analysis. Our findings revealed that AZT inhibited HIV-1 replication, and its treatment interruption led to the reactivation of viral replication. This reactivation occurred through the recruitment of host transcription factors, including NFAT, NF-κBp65, Ap-1, and Sp-1. These factors facilitated HIV production via TCR-related pathways, activation of p-TEFb pathways for transcription elongation, and upregulation of Jak/Stat pathways for viral enhancement. Furthermore, we demonstrated that PMA treatment increased the levels of these transcription factors through the activation of TCR-related signaling pathways in HIV-1 infected Jurkat cells, irrespective of the AZT treatment status. PMA also induced cell death through both extrinsic and intrinsic apoptotic signaling pathways, as well as autophagy. These results suggest that PMA effectively employs the shock-and-kill approach in HIV-1 infected Jurkat cells and highlight the potential of PKC pathway activators as promising LRAs.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"13 11","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140277928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0