Cell and Tissue Biology最新文献

{"title":"Prospects for the Use of Cell Cultures in Modeling Myocardial Diseases: Hypertrophic Cardiomyopathy","authors":"A. L. Klass, M. I. Shadrina, P. A. Slominsky, E. V. Filatova","doi":"10.1134/s1990519x24700305","DOIUrl":"https://doi.org/10.1134/s1990519x24700305","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>The use of various model organisms has made a huge contribution to understanding the causes and mechanisms of disease development and the study of pathological processes occurring during the development of diseases of the human cardiovascular system, and, in particular, hypertrophic cardiomyopathy (HCM). The optimal solution in the study of primary molecular disturbances is the use of cellular models such as induced pluripotent stem cells (iPSCs), primary rodent cardiomyocytes (CMs), and immortalized lines. In this review, we have focused on the most commonly used cell models, including freshly isolated adult and neonatal rodent CMs, and on the commercially available immortalized cell lines (HL-1, AC16, and H9c2). In order to assess the adequacy of these lines as CM models for studying human myocardial pathologies, a comparative analysis of phenotypic characteristics (morphology, metabolism, calcium homeostasis, etc.) and the nuances of practical use (availability, response to hypertrophic inducers, transfection, etc.) was carried out. The latest published data on the use of these models to assess the pathogenicity of HCM-associated mutations, as well as to screen the effectiveness of developed therapeutic drugs, are also summarized.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"32 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141931653","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}

{"title":"A Multi-Omics Analysis to Investigate the Co-Occurrence of Psoriasis and Crohn’s Diseases","authors":"Mohsen Danaeifar","doi":"10.1134/s1990519x24700317","DOIUrl":"https://doi.org/10.1134/s1990519x24700317","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Psoriasis is a chronic autoimmune condition that causes rapid buildup of skin cells. Crohn’s disease is a chronic inflammatory bowel disease that affects the gastrointestinal tract. Psoriasis and Crohn’s disease are both chronic inflammatory disorders that are believed to share some common genetic and environmental risk factors. Aim of this study is to investigate possible link between psoriasis and Crohn’s disease through multi-omics approach. To obtain transcriptomics data of psoriasis and Crohn’s disease, four and three datasets of gene expression omnibus (GEO), as well as two proteomics datasets for each disease were used. Gene expression analysis, protein-protein network analysis and pathway enrichment were performed for differentially expressed genes and proteins. The main enriched pathway in psoriasis is interleukin-27-mediated signaling pathway, while for Crohn’s disease it was tryptophan catabolic process to kynurenine. The results showed that coding genes of IL-8, IL-10 and IL-17A are the main link between psoriasis and Crohn’s disease and in this link, Th1 plays an important role. On the other hand, it was also shown that METTL7A facilitates the infiltration of Th1 cells into the skin and colon tissue. Through this study, important molecules that involved in co-occurrence of the psoriasis and Crohn’s disease are introduced.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"96 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141931654","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}

{"title":"α-Tocopheryl Succinate Induces ER Stress, Disruption of Lipid Metabolism, and Apoptosis in a Culture of Normal and Tumor Cells of Epidermal Origin","authors":"M. A. Savitskaya, I. I. Zakharov, A. A. Saidova, E. A. Smirnova, G. E. Onishchenko","doi":"10.1134/s1990519x2470038x","DOIUrl":"https://doi.org/10.1134/s1990519x2470038x","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Vitamin E succinate (VES) is a potential antitumor agent known for its targeted effect on the mitochondria of tumor cells. However, data on the proapoptotic mechanism of action of VES are ambiguous, and the effect of VES on normal nontumorigenic cells has not been fully studied. Previously, it was possible to demonstrate the induction of apoptosis by the mitochondrial mechanism under the action of VES on human epidermoid carcinoma A431 cells. The purpose of this work is to investigate the effect of VES on nontumorigenic cells and to identify common mechanisms that are characteristic of both normal and tumor cells, as well as mechanisms that manifest themselves only in one of the categories of cells. To achieve this goal, the effect of VES on such organelles as endoplasmic reticulum (ER) and the Golgi apparatus and the expression of genes associated with ER stress were analyzed, and also the reactive oxygen species (ROS) content and accumulation of lipid droplets in the cytoplasm in human epidermoid carcinoma A431 cells and HaCaT immortalized human keratinocytes were assessed. It was shown that, in cells of both lines, there are signs of ER stress, the content of ROS and lipid inclusions and the number of apoptotic cells increase. At the same time, the key difference between the mechanisms of induction of apoptotic death of A431 and HaCaT cells under the influence of VES lies in the reaction of mitochondria: in A431 cells, apoptotic death is triggered by the mitochondrial mechanism, while HaCaT cells enter apoptosis without the participation of mitochondria. Thus, the targets of VES on normal and tumor cells may differ and, possibly, can complement each other in inducing apoptosis.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"46 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141931660","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}

{"title":"Tricyclic Antidepressant Amitriptyline Suppresses Ca2+ Responses in Rat Peritoneal Macrophages","authors":"L. S. Milenina, Z. I. Krutetskaya, V. G. Antonov, N. I. Krutetskaya","doi":"10.1134/s1990519x24700378","DOIUrl":"https://doi.org/10.1134/s1990519x24700378","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Amitriptyline is a tricyclic antidepressant widely used in clinical practice for the treatment of an-xiety and depression and chronic pain. These drugs have a multifaceted effect on cellular processes. One of their targets is sigma-1 receptors. Sigma-1 receptors are molecular chaperones located in the membrane of the endoplasmic reticulum; they are characterized by a unique structure and pharmacological profile. Sigma-1 receptors regulate many cellular processes in health and disease, including processes of Ca²⁺ signaling. Using Fura-2AM fluorescent Ca²⁺ probe, we showed for the first time that sigma-1 receptor agonist, the antidepressant amitriptyline, significantly suppresses Ca²⁺ mobilization from the intracellular Ca²⁺ stores and subsequent store-dependent Ca²⁺ entry into cells caused by inhibitors of endoplasmic Ca²⁺ ATPases thapsigargin and cyclopiazonic acid, as well as the disulfide-containing immunomodulators glutoxim and molixan, in rat peritoneal macrophages. The results indicate the participation of sigma-1 receptors in the complex signaling cascade caused by glutoxim or molixan, leading to an increase in intracellular Ca²⁺ concentration in macrophages. Data also indicate that sigma-1 receptors participate in the regulation of store-dependent Ca²⁺ entry in macrophages.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141931661","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}

{"title":"PTEN Knockout Causes Premature Senescence of Human Endometrial Stromal Cells","authors":"P. S. Parfenova, P. I. Deryabin, D. Yu. Pozdnyakov, A. V. Borodkina","doi":"10.1134/s1990519x24700330","DOIUrl":"https://doi.org/10.1134/s1990519x24700330","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>One protective mechanism against neoplastic transformation of cells in response to oncogenic stimuli is cellular senescence. However, the ability of cells to activate this protective reaction depends on their nature and is not characteristic of all cell types. In this study, we studied the response of human endometrial stromal cells (EnSC-EnSC) to a classic oncogenic stimulus—inactivation of the tumor suppressor <i>PTEN</i>. Using CRISPR/Cas9 targeted genome editing technology, we were able to obtain an EnSC line with <i>PTEN</i> gene knockout. We showed that a decrease in the expression of <i>PTEN</i> leads to loss of proliferative activity, hypertrophy, accumulation of lipofuscin, and disruption of the redox balance of cells. The totality of the identified signs testifies in favor of the induction of premature senescence in EnSCs with <i>PTEN</i> knockout. When studying the molecular mechanisms, we established the key role of the PI3K/AKT signaling pathway in the implementation of the EnSC senescence program under conditions of <i>PTEN</i> knockout. Inhibition of this signaling pathway using the substance LY294002 prevented both the phenotypic manifestations of premature senescence and cell cycle arrest in <i>PTEN</i>-cell knockout. Thus, the development of premature senescence in conditions of reduced expression of the <i>PTEN</i> tumor suppressor can be considered a protective mechanism that prevents the malignant transformation of EnSCs.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141931656","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}

{"title":"Role of Calcium Channels in Glucose Uptake Regulation in the In Vitro Model of Polarized Intestinal Epithelium","authors":"D. E. Bobkov, A. V. Lukacheva, L. V. Kever, V. V. Furman, S. B. Semenova","doi":"10.1134/s1990519x24700366","DOIUrl":"https://doi.org/10.1134/s1990519x24700366","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Glucose is the main energy substrate that ensures metabolic processes in the human and animal bodies. Impaired carbohydrate metabolism is often associated with obesity and concomitant diseases, such as cardiovascular diseases, arterial hypertension, insulin resistance, etc. Current data indicate that intestinal glucose absorption is coupled with Ca²⁺ influx, but additional research is needed to confirm this interaction. We used a cellular model of human intestinal epithelium to elucidate the role of Ca²⁺ channels in the regulation of glucose absorption. The results of immunofluorescence and immunoelectron microscopy showed that high cellular glucose loading (50 mM) leads to an increase in the density of TRPV6 calcium channels on the apical membrane of the intestinal epithelium. The level of the calcium sensor STIM1, responsible for store-dependent calcium entry (SOCE), on the contrary, showed a decrease when Caco-2 cells were overloaded with glucose, which was accompanied by a decrease in SOCE. Excessive saturation of Caco-2 cells with glucose also led to a decrease in the expression level of the NF-κB transcription factor p65 subunit responsible for the expression of STIM1. The results showed that Ca²⁺ channels are not only involved in the regulation of glucose uptake, but may themselves be under the control of glucose.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"303 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141931658","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}

{"title":"The Role of Clycodelin in Conversion of CD11b+ Cells to MDSCs and Regulation of Their Functional Activity","authors":"K. Yu. Shardina, S. A. Zamorina, M. S. Bochkova, V. P. Timganova, S. V. Uzhviyuk, M. B. Raev","doi":"10.1134/s1990519x24700342","DOIUrl":"https://doi.org/10.1134/s1990519x24700342","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Glycodelin (Gd) has pronounced immunomodulatory properties and participates in the development of immune tolerance during pregnancy. The role of recombinant Gd in physiological (0.2 and 2 μg/mL) and superphysiological (10 μg/mL) concentrations in the regulation of differentiation and functional activity of human myeloid-derived suppressor cells (MDSCs) was investigated in vitro. MDSCs were obtained from peripheral blood CD11b⁺ cells of healthy donors by two-step induction (IL-1β + granulocyte–monocyte colony-stimulating factor (GM-CSF) and lipopolysaccharide). The effect of Gd on the level of polymorphonuclear MDSCs (PMN-MDSCs) and monocyte MDSCs (M-MDSCs) was assessed. The intracellular level of indoleamine 2,3-dioxygenase (IDO) and arginase 1 (Arg1), as well as the cytokine profile in cultures of these cells, was measured. In general, the conversion of CD11b⁺ cells into MDSCs has the following features: as a result of cytokine induction, predominantly M-MDSCs are generated, but not PMN-MDSCs, and the level of Arg1 is practically not detected. It was found that Gd increased the number of M-MDSCs at concentrations of 2 and 10 μg/mL. It was shown that Gd did not affect the content of Arg1, but increased the number of MDSCs expressing IDO (10 μg/mL). Gd also modulated the cytokine profile of CD11b⁺ cells (at a physiological concentration of 2 μg/mL), suppressing IL-19, IL-26, and TWEAK/TNFsF12 production and, at a supraphysiological concentration, the production of IFN-α2 and IL-26.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141931657","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}

{"title":"Overexpression of Discoidin Domain Receptor 1 Is Associated with Tumor Size in Esophageal Squamous Cell Carcinoma","authors":"Afsaneh Shafiei, Seyyed Mehdi Jafari, Marie Saghaeian Jazi, Mahmoud Pourjam, Jahanbakhsh Asadi","doi":"10.1134/s1990519x24700226","DOIUrl":"https://doi.org/10.1134/s1990519x24700226","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Background<i>.</i> Discoidin domain receptor 1 (DDR1) is confirmed as a member of the transmembrane receptor tyrosine kinase (RTK) superfamily, which plays an influential role in various cancers. Increasing evidence has suggested that DDR1 is plays role in cancer progression and metastasis. However, DDR1 function and the underlying mechanism of DDR1 receptor signaling pathways is largely unknown, especially in esophageal squamous cell carcinoma (ESCC). Methods and results<i>.</i> We obtained 42 paired samples of ESCC tumors (<i>N</i> = 21) and adjacent normal tissues (<i>N</i> = 21) from newly diagnosed ESCC patients. In this study, the expression of DDR1 in esophageal cancer was retrieved based on the GENT2, OncoDB databases. AlsoqRT-PCR experiments was used to measure DDR1 expression experimentally in ESCC tissues compared to adjacent non-tumor tissues (NTs). Moreover, the correlation between the expression of DDR1 and clinic pathologic factors was analyzed. The diagnostic significance of the results was subsequently evaluated utilizing the receiver operating characteristic (ROC) curve. The result showed that mRNA expression of DDR1 was up-regulated in ESCC tissues compared with NTs (<i>p</i> = 0.0001). Statistical analysis revealed that DDR1 expression was significantly higher in samples with a tumor size of more than five centimeters (<i>p</i> = 0.02). The ROC curve analysis indicated that DDR1 expression level in tissue potentially have high accuracy for diagnosing ESCC compared with adjacent non-tumor tissues NTs (AUC = 0.92, Specificity = 84%, sensitivity = 96%). Conclusions<i>.</i> Our findings suggest that overexpression of the DDR1 might play a function in promoting cancer and tumor size. Moreover, DDR1 can potentially act as a novel biomarker for identifying ESCC patients, indicating the potential of this receptor for ESCC-targeted therapeutics.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"20 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141254535","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}

{"title":"Analysis of Slow Inactivation of Nav1.5 Channels in the Development of Hereditary Heart Pathology","authors":"A. K. Zaitseva, K. I. Perepelina, A. A. Kostareva","doi":"10.1134/s1990519x24700263","DOIUrl":"https://doi.org/10.1134/s1990519x24700263","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Cardiac voltage-gated Na_v1.5 sodium channels are responsible for initiation and propagation of action potentials in cardiomyocytes. Na_v1.5 dysfunction may be due to both pathogenic variants in the gene itself <i>SCN5A</i>, encoding Na_v1.5, and genetic variants in the genes of other proteins that regulate its activity and transport. The change of different phases of the action potential is determined by the strict temporal organization of activation and inactivation of various ion channels. Transitions between functional states of the channel, including the transition to the slow inactivation state, can be influenced by a variety of factors and proteins interacting with the channel. Despite the fact that the process of slow inactivation of the channel has been known for several decades, its role in the mechanism of development of hereditary heart pathology remains unclear. In this work, using the method of local potential fixation (patch clamp) in a lead from a whole cell, we investigated changes in the process of slow inactivation of Na_v1.5 under the influence of various mutations in structural genes (<i>DSP</i>-H1684R, <i>LMNA</i>-R249Q, <i>FLNC</i>-R1267Q, and <i>FLNC</i>-V2264M), associated with genetically determined myocardial pathology, leading to dysfunction of cardiomyocytes. We used a model of cardiomyocytes differentiated from induced pluripotent stem cells (CM-iPSCs) and demonstrated enhancement of slow channel inactivation in a model of CM-iPSCs obtained from patients with a cardiomyopathy phenotype combined with ventricular arrhythmias. Thus, the presented work contributes to understanding the role of the process of slow inactivation of Na_v1.5 in the mechanism of development of heart pathology.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"44 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141254630","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}

{"title":"Interaction of pRb and β-Catenin in Cancer and Normal Human Prostate Tissue","authors":"V. M. Ryabov, N. I. Tyapkin, A. P. Rodimtsev, O. G. Lyublinskaya, I. V. Guzhova, B. V. Popov","doi":"10.1134/s1990519x24700238","DOIUrl":"https://doi.org/10.1134/s1990519x24700238","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Prostate cancer (PCa) is one of the most common oncological diseases, which passes through two stages in its development: localized PCa and castration-resistant PCa (CR-PCa). The first stage—localized prostate cancer—can proceed indefinitely in a dormant form that does not require active medical intervention, or suddenly turn into an aggressive metastatic form (CR-PCa)<b>,</b> ending in rapid death. The pathogenesis of the transition of the dormant form of PCa to the metastatic form remains not fully understood. The signaling pathways of tumor suppressor pRb and proto-oncogene β-catenin are probably the most involved in the pathogenesis of prostate cancer, but the role of their interaction has not been studied. The publication on the pathogenesis of tumors in other tissues suggests that pRb may lose some properties of a tumor suppressor at the initial stage of PCa development due to its interaction with β-catenin that enables tumor cells to gain competitive advantages for reproduction. In this work, we showed that the genes <i>RB</i> and β-catenin (<i>CTNNB1</i>) are expressed in tumor and normal prostate tissue. Unlike β-catenin, pRb is not detected by immunoblotting in tumor and normal prostate tissue, but is easily detected in this way in extracts of control T98G cells. Co-immunoprecipitation with antibodies to pRb from extracts of tumor and normal prostate tissue makes it possible to detect this protein and β-catenin by subsequent immunoblotting, which indicates the physical interaction of these proteins in prostate tissue. On the other hand, immunoprecipitation of β-catenin with antibodies to its C-terminal fragment does not make it possible to detect this protein in prostate extracts by subsequent immunoblotting using the same antibodies. In contrast to prostate tissue, β-catenin was readily detected by immunoprecipitation coupled with immunoblotting in extracts of control T98G cells. The obtained data suggest that pRb and β-catenin physically interact with each other in cells of different tissue specificity. In T98G cells, this interaction probably occurs through the C-terminal fragment of β-catenin, but in prostate cells it occurs in a different way, since the C fragment of β-catenin is shielded from such interaction, possibly due to its physical association with pRb.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"68 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141254537","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}