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Retraction: Baicalin suppresses lung cancer growth by targeting PDZ-binding kinase/T-LAK cell-originated protein kinase. 撤回:黄芩苷通过靶向pdz结合激酶/T-LAK细胞源蛋白激酶抑制肺癌生长。
IF 4.5 3区 生物学
Bioscience Reports Pub Date : 2026-10-21 DOI: 10.1042/BSR20181692_RET
Xin Diao, Danfen Yang, Yu Chen, Wentian Liu
{"title":"Retraction: Baicalin suppresses lung cancer growth by targeting PDZ-binding kinase/T-LAK cell-originated protein kinase.","authors":"Xin Diao, Danfen Yang, Yu Chen, Wentian Liu","doi":"10.1042/BSR20181692_RET","DOIUrl":"10.1042/BSR20181692_RET","url":null,"abstract":"","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":"46 10","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13673171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Metataxonomic strategy to decipher gut bacteriome biomarkers of type 2 diabetes and obesity in Tunisian population. 突尼斯人群中2型糖尿病和肥胖症肠道细菌组生物标志物的元分类策略
IF 4.5 3区 生物学
Bioscience Reports Pub Date : 2026-10-21 DOI: 10.1042/BSR20260157
Meriem Fassatoui, Thierry Pedron, Nadia Kheriji, Meriem Hechmi, Hamza Dallali, Haifa Jmel, Henda Jamoussi, Abdelmajid Abid, Philippe J Sansonetti, Rym Kefi
{"title":"Metataxonomic strategy to decipher gut bacteriome biomarkers of type 2 diabetes and obesity in Tunisian population.","authors":"Meriem Fassatoui, Thierry Pedron, Nadia Kheriji, Meriem Hechmi, Hamza Dallali, Haifa Jmel, Henda Jamoussi, Abdelmajid Abid, Philippe J Sansonetti, Rym Kefi","doi":"10.1042/BSR20260157","DOIUrl":"10.1042/BSR20260157","url":null,"abstract":"<p><p>Metabolic disorders are multifactorial diseases and major global health concerns, with many individuals worldwide responding inadequately to treatments. The gut bacteriome regulates metabolism and offers therapeutic potential; however, research from North Africa remains scarce despite the growing prevalence of non-communicable diseases in the region. This study examines gut bacterial profiles of Tunisian type 2 diabetic (T2D), obese (OB), and non-diabetic (ND) individuals within the framework of personalized medicine. Ninety-five participants were enrolled [33 ND, 26 T2D, 26 T2D with obesity and cardiovascular complications (T2D_OBCV) and 10 OB]. Bacterial 16S rDNA V3-V4 regions were sequenced on Illumina MiSeq and analyzed using the QIIME 2 pipeline. Obese subjects exhibited gut dysbiosis with lower Akkermansia (P=0.02) and Ligilactobacillus (P=0.04) levels, an enrichment of Bifidobacterium (P=0.004), as well as Sutterella (P=0.03) and Erysipelatoclostridium (P=0.02). However, the gut bacteriome landscape of T2D patients reveals differences in the distribution of Shigella (P=0.01) highly abundant in the intestine, and a depletion of Clostridia vadin BB 60 group (P=0.02) and Oscillospiraceae UCG 005 (P=0.01). Noting that the gut bacteriome of T2D_OBCV patients is characterized by a depletion of Asteroleplasma (P=0.01), Oscillospiraceae UCG 005 (P=0.02), Eubacterium ruminantium group (P=0.0007) and Romboutsia (P=0.002) beside an enrichment of Fusicatenibacter (P=0.02). Gut bacteriome alterations in Tunisian T2D and obese subjects may serve as metabolic biomarkers.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13673178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149023416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 unorthodox aquaporin-12L ortholog is essential for oogenesis in the crustacean Artemia franciscana. 非正统的水通道蛋白- 12l同源体是甲壳类动物Artemia franciscana卵发生所必需的。
IF 4.5 3区 生物学
Bioscience Reports Pub Date : 2026-10-21 DOI: 10.1042/BSR20260496
Ángel Rey-Alfonso, François Chauvigné, Roderick Nigel Finn, Joan Cerdà
{"title":"The unorthodox aquaporin-12L ortholog is essential for oogenesis in the crustacean Artemia franciscana.","authors":"Ángel Rey-Alfonso, François Chauvigné, Roderick Nigel Finn, Joan Cerdà","doi":"10.1042/BSR20260496","DOIUrl":"10.1042/BSR20260496","url":null,"abstract":"<p><p>The intracellular unorthodox aquaporins, AQP11 and AQP12, remain the least characterized members of the aquaporin superfamily. Mammalian and teleost AQP12 channels have recently been established as polytransporters in native membranes. They are localized intracellularly in pancreatic acinar cells and considered to play roles in zymogen granule maturation and exocytosis. In contrast with the vertebrate channels, the permeability properties and physiological roles of invertebrate AQP12-like (Aqp12L) orthologs are completely unknown. Here, we report that the Aqp12L channel from the extremophile crustacean Artemia franciscana is specifically targeted to the membrane of the yolk platelets (YPs) when heterologously expressed in frog (Xenopus laevis) oocytes, as recently reported for the vertebrate orthologs. Using YPs isolated from A. franciscana Aqp12L-expressing frog oocytes, we further show that this channel can transport water, H2O2, ammonia, and urea but not glycerol. Immunostaining of the A. franciscana ovary using a specific Aqp12L antibody revealed that the in vivo localization of the channel also occurs in the YP membranes of vitellogenic oocytes. RNAi-mediated silencing of Aqp12L substantially reduces the offspring output of both ovoviviparous and oviparous females through the impairment of oocyte vitellogenesis (oocyte growth) and the premature activation of ovarian apoptotic and atretic pathways. These findings provide the first direct evidence demonstrating that invertebrate Aqp12L is a functional polytransporter with an essential role in crustacean oogenesis.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13673172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149103507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Design of short-sequenced collagen type III-derived peptides with GPR56 dependent biological activity. 具有GPR56依赖性生物活性的iii型胶原衍生短序列肽的设计。
IF 4.5 3区 生物学
Bioscience Reports Pub Date : 2026-10-16 DOI: 10.1042/BSR20250320
Israa Mohammed Al-Amily, Fariborz Parandeh, Pontus Duner, Marie Sjögren, Albert Salehi
{"title":"Design of short-sequenced collagen type III-derived peptides with GPR56 dependent biological activity.","authors":"Israa Mohammed Al-Amily, Fariborz Parandeh, Pontus Duner, Marie Sjögren, Albert Salehi","doi":"10.1042/BSR20250320","DOIUrl":"https://doi.org/10.1042/BSR20250320","url":null,"abstract":"<p><p>We have previously shown that activation of G protein-coupled receptor 56 (GPR56) by its endogenous ligand collagen type III (Coll III) improves pancreatic β-cell function and potentiates glucose-stimulated insulin secretion (GSIS). In the current study, alignment of Coll III and GPR56 genomic DNA revealed three complementary nucleotide regions, enabling the design of three short peptides (NQGCKL.NH2, H.LLSSR.NH2 and NH2.GYYCG.COOH). The peptides in double or triple combinations markedly increased cellular cAMP levels, enhanced GSIS, and improved cell viability both in human (EndoC βH1 cells) and rat pancreatic β-cell lines (INS-1 832/13 cells). These effects were markedly absent in GPR56-knockdown (GPR56-KD) cells, supporting receptor-dependent specificity. The peptide mixtures also counteracted cytokine- and glucotoxicity-induced cellular stress, restoring cAMP generation and insulin secretion. Comparable effects were not observed with dapagliflozin while glibenclamide decreased cell viability under similar conditions. In hepatic cell lines (HepG2, Hep1-6), peptide combinations enhanced cell survival in a GPR56-dependent manner, consistent with a broader role of GPR56 in metabolic regulation. Collectively, the data identify three short sequence collagen III-derived peptides whose biological effects are dependent on GPR56 expression and support their further investigation as tools for studying GPR56-associated cellular signaling for the future in vivo validation.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
IGFBP2 attenuates high glucose-induced endothelial dysfunction through PI3K/Akt/eNOS pathway activation. IGFBP2通过激活PI3K/Akt/eNOS通路减弱高糖诱导的内皮功能障碍。
IF 4.5 3区 生物学
Bioscience Reports Pub Date : 2026-10-08 DOI: 10.1042/BSR20260182
Xiaoyu Song, Wentao Zhong, Chengqian Chen, Hao Zheng, Zhuo Li
{"title":"IGFBP2 attenuates high glucose-induced endothelial dysfunction through PI3K/Akt/eNOS pathway activation.","authors":"Xiaoyu Song, Wentao Zhong, Chengqian Chen, Hao Zheng, Zhuo Li","doi":"10.1042/BSR20260182","DOIUrl":"https://doi.org/10.1042/BSR20260182","url":null,"abstract":"<p><p>Endothelial dysfunction induced by hyperglycemia is a key event in diabetic vascular complications and is closely associated with impaired PI3K/Akt/eNOS signaling. Insulin-like growth factor-binding protein 2 (IGFBP2) has been implicated in metabolic regulation and cell survival, but its role in high glucose-induced endothelial injury remains unclear. In this study, human umbilical vein endothelial cells (HUVECs) were exposed to high glucose (HG, 33 mM) for 24 hours and then treated with recombinant human IGFBP2 (rhIGFBP2, 200 ng/mL) for 60 minutes. HG reduced Akt/eNOS phosphorylation and nitric oxide (NO) production, increased the expression of ICAM-1, VCAM-1, and SELE, promoted IL-6, IL-8, and MCP-1 secretion, and enhanced apoptosis. rhIGFBP2 attenuated these HG-induced changes by restoring PI3K/Akt/eNOS signaling and NO production, reducing inflammatory activation, and decreasing apoptotic cell percentage. The effect of rhIGFBP2 on Akt/eNOS phosphorylation and NO production was broadly comparable to that of insulin under HG conditions. HG also increased p38 MAPK phosphorylation, whereas rhIGFBP2 showed only a non-significant decreasing trend. Importantly, PI3K inhibition with LY294002 abolished rhIGFBP2-induced Akt/eNOS activation, supporting the involvement of the PI3K/Akt/eNOS pathway. These findings suggest that IGFBP2 protects against HG-induced endothelial dysfunction mainly by activating PI3K/Akt/eNOS signaling and may represent a potential mediator of endothelial protection under diabetic conditions.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A Thermally Processed Cafeteria Diet Reproducibly Mimics Early Metabolic Syndrome Through Obesogenic, Inflammatory, and Adipose Dysfunctions in Wistar Rats. 在Wistar大鼠中,热处理的自助餐厅饮食可通过肥胖、炎症和脂肪功能障碍再现模仿早期代谢综合征。
IF 4.5 3区 生物学
Bioscience Reports Pub Date : 2026-10-02 DOI: 10.1042/BSR20260388
Susana Barbosa Ribeiro, Rômulo Camilo de Oliveira Melo, Lucas Vinicius Souza de Carvalho, Arnóbio Antônio da Silva Júnior, Raimundo Fernandes de Araújo Júnior, Amanda Silveira da Silva, Gabrielle Marques de Paiva, Vinicius Barreto Garcia, Ana Heloneida de Araújo Morais, Ana Júlia Felipe Camelo Aguiar, Caroline Addison Carvalho Xavier de Medeiros, Maiara De Morais, Bruna Rafaela Martins Dos Santos, Rafael Lino Mokwa, Francisco Canindé de Souza Júnior, Maíra Conceição Jerônimo de Souza Lima, Ciro Dantas Soares, Aurigena Antunes de Araújo
{"title":"A Thermally Processed Cafeteria Diet Reproducibly Mimics Early Metabolic Syndrome Through Obesogenic, Inflammatory, and Adipose Dysfunctions in Wistar Rats.","authors":"Susana Barbosa Ribeiro, Rômulo Camilo de Oliveira Melo, Lucas Vinicius Souza de Carvalho, Arnóbio Antônio da Silva Júnior, Raimundo Fernandes de Araújo Júnior, Amanda Silveira da Silva, Gabrielle Marques de Paiva, Vinicius Barreto Garcia, Ana Heloneida de Araújo Morais, Ana Júlia Felipe Camelo Aguiar, Caroline Addison Carvalho Xavier de Medeiros, Maiara De Morais, Bruna Rafaela Martins Dos Santos, Rafael Lino Mokwa, Francisco Canindé de Souza Júnior, Maíra Conceição Jerônimo de Souza Lima, Ciro Dantas Soares, Aurigena Antunes de Araújo","doi":"10.1042/BSR20260388","DOIUrl":"https://doi.org/10.1042/BSR20260388","url":null,"abstract":"<p><p>The obesogenic nutrient composition and processing characteristics of ultra-processed foods may contribute to metabolic dysfunction. This study evaluated a standardized cafeteria diet, alone or combined with low-dose streptozotocin (STZ), in male Wistar rats. Animals (n = 32) were allocated to Healthy Control, STZ (35 mg/kg), Cafeteria Diet (CAF), and CAF+STZ groups. The diet contained standard chow, condensed milk, refined sugar, hydrogenated fat, soybean oil, and chocolate-filled biscuits, homogenized and thermally processed at 180 °C. After 102 days, anthropometric, metabolic, inflammatory, gene expression, microbiota, and histopathological parameters were assessed. CAF induced a marked obesogenic phenotype, with increased body weight (+172.3%) and abdominal circumference (+38.7%; p < 0.01). CAF showed hyperglycemia (median glucose, 403 mg/dL) and higher HOMA-IR than Healthy Control (p < 0.01); CAF+STZ also showed increased HOMA-IR (p < 0.05). CAF increased IL-1β and IL-6 (p < 0.05), triglycerides, adipocyte hypertrophy (p < 0.01), and adipose Leptin expression (p < 0.05), while reducing muscle Slc2a4/GLUT4 expression (p < 0.01). Liver, kidney, and pancreatic histopathological scores did not differ significantly. Gut microbiota showed marked compositional imbalance and low taxonomic evenness, with Firmicutes (99.83%), Ligilactobacillus (99.36%), and Lactobacillaceae (99.52%) predominating, while Enterobacteriaceae represented 0.14%. Despite no reduction in Shannon or Simpson indices, extreme Ligilactobacillus dominance indicated a restricted and uneven community. Overall, the cafeteria diet reproduced obesity-associated metabolic dysfunction, characterized by hyperglycemia, insulin resistance, inflammation, adipocyte hypertrophy, altered glucose and leptin expression, and substantial microbiota restructuring.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149103443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Retraction: The resistant effect of SIRT1 in oxidative stress-induced senescence of rat nucleus pulposus cell is regulated by Akt-FoxO1 pathway. 撤回:SIRT1在氧化应激诱导的大鼠髓核细胞衰老中的抵抗作用是通过Akt-FoxO1通路调控的。
IF 4.5 3区 生物学
Bioscience Reports Pub Date : 2026-09-16 DOI: 10.1042/BSR20190112_RET
Junsheng He, Ailiang Zhang, Zhiwen Song, Shiwu Guo, Yuwei Chen, Zhiyuan Liu, Jinlong Zhang, Xu Xu, Jinbo Liu, Lei Chu
{"title":"Retraction: The resistant effect of SIRT1 in oxidative stress-induced senescence of rat nucleus pulposus cell is regulated by Akt-FoxO1 pathway.","authors":"Junsheng He, Ailiang Zhang, Zhiwen Song, Shiwu Guo, Yuwei Chen, Zhiyuan Liu, Jinlong Zhang, Xu Xu, Jinbo Liu, Lei Chu","doi":"10.1042/BSR20190112_RET","DOIUrl":"10.1042/BSR20190112_RET","url":null,"abstract":"","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":"46 9","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148910646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Engineering a genetic construct to express soluble proteins tethered to the cell membrane. 设计一种基因结构来表达附着在细胞膜上的可溶性蛋白质。
IF 4.5 3区 生物学
Bioscience Reports Pub Date : 2026-09-16 DOI: 10.1042/BSR20260216
Alejandro Ronco-Campaña, John Simms, Alan D Goddard, Alice J Rothnie
{"title":"Engineering a genetic construct to express soluble proteins tethered to the cell membrane.","authors":"Alejandro Ronco-Campaña, John Simms, Alan D Goddard, Alice J Rothnie","doi":"10.1042/BSR20260216","DOIUrl":"10.1042/BSR20260216","url":null,"abstract":"<p><p>Synthetic biology has significantly grown and developed in the last decades, allowing its implementation in a wide variety of fields and applications. However, there is a lack of versatile, modular tools that allow the expression of soluble proteins anchored to the cell membrane, which could be useful in a range of applications. Therefore, using a combination of computational simulations and experimental validation, we designed a genetic construct for the expression of soluble proteins tethered to the cell membrane. Using green fluorescent protein as a model soluble protein, we demonstrated that it was successfully tethered to the cell membrane and that it could be incorporated into polymer lipid nanodiscs and purified through the histidine tag. Replacement of the reporter gene with another gene of interest could lead to its application in a wide variety of fields, from creating artificial signalling or enzymatic cascades to studying lipid and protein dynamics in the cell membrane.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570435/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148787794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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: LncRNA TUG1 promotes the progression of colorectal cancer via the miR-138-5p/ZEB2 axis. 回撤:LncRNA TUG1通过miR-138-5p/ZEB2轴促进结直肠癌的进展。
IF 4.5 3区 生物学
Bioscience Reports Pub Date : 2026-09-16 DOI: 10.1042/BSR20201025_RET
Zhenkun Yan, Miaomiao Bi, Qiyu Zhang, Yumei Song, Sen Hong
{"title":"Retraction: LncRNA TUG1 promotes the progression of colorectal cancer via the miR-138-5p/ZEB2 axis.","authors":"Zhenkun Yan, Miaomiao Bi, Qiyu Zhang, Yumei Song, Sen Hong","doi":"10.1042/BSR20201025_RET","DOIUrl":"10.1042/BSR20201025_RET","url":null,"abstract":"","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":"46 9","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148910640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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: TRPM8 facilitates proliferation and immune evasion of esophageal cancer cells. 收缩:TRPM8促进食管癌细胞增殖和免疫逃逸。
IF 4.5 3区 生物学
Bioscience Reports Pub Date : 2026-09-16 DOI: 10.1042/BSR20191878_RET
Xinyan Lan, Jun Zhao, Chunjing Song, Qiuxiang Yuan, Xiaojun Liu
{"title":"Retraction: TRPM8 facilitates proliferation and immune evasion of esophageal cancer cells.","authors":"Xinyan Lan, Jun Zhao, Chunjing Song, Qiuxiang Yuan, Xiaojun Liu","doi":"10.1042/BSR20191878_RET","DOIUrl":"10.1042/BSR20191878_RET","url":null,"abstract":"","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":"46 9","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148910668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
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