Bioscience Reports最新文献_第9页

Retraction: HDAC regulates the diabetic vascular endothelial dysfunction by targeting MnSOD. 缩回：HDAC通过靶向MnSOD调控糖尿病血管内皮功能障碍。

IF 4.5 3区生物学

Bioscience Reports Pub Date : 2026-04-22 DOI: 10.1042/BSR20181042_RET

Zehao Liu, Qian Hou, Ke Hu, Xiaofeng Liu, Jiao Quan

引用次数: 0

The role of DOT1L in the proliferation and prognosis of gastric cancer. DOT1L在胃癌增殖及预后中的作用。

IF 4.5 3区生物学

Bioscience Reports Pub Date : 2026-04-22 DOI: 10.1042/BSR20193515_RET

Jun Qian, Zaozhi Song, Zhuoli Wei, Qingkang Wang, Xinxin Zhang, Xiaoying Tao, Nan Wu, Xue Liu

引用次数: 0

Retraction: ANRIL promotes chemoresistance via disturbing expression of ABCC1 by regulating the expression of Let-7a in colorectal cancer. 撤回：ANRIL通过调节Let-7a在结直肠癌中的表达，干扰ABCC1的表达，从而促进化疗耐药。

IF 4.5 3区生物学

Bioscience Reports Pub Date : 2026-04-22 DOI: 10.1042/BSR20180620_RET

Pengfei Liu, Wei Duan, Zhen Zhang, Lifeng Feng

引用次数: 0

Using a bioluminescence resonance energy transfer caspase biosensor to study caspase-3 cleavage site specificity. 利用生物发光共振能量转移（BRET2） caspase生物传感器研究caspase-3切割位点特异性。

IF 4.5 3区生物学

Bioscience Reports Pub Date : 2026-04-22 DOI: 10.1042/BSR20254030

Véronique Blais, Jean-Bernard Denault

{"title":"Using a bioluminescence resonance energy transfer caspase biosensor to study caspase-3 cleavage site specificity.","authors":"Véronique Blais, Jean-Bernard Denault","doi":"10.1042/BSR20254030","DOIUrl":"10.1042/BSR20254030","url":null,"abstract":"In its simplest representation, apoptosis is a two-step peptidase cascade in which initiator caspases (caspases-8, -9, and -10) activate executioner caspases (caspases-3, -6, and -7). Although many intricacies exist-such as the proteolysis of initiator caspases by executioner caspases, which further regulates their activity-apoptotic pathways ultimately converge on the activation of caspase-3, the most proteolytically proficient member of the family. This central role has led to the development of numerous enzymatic assays to detect caspase-3 activity, its activation, and the cleavage of hallmark substrates, such as poly(ADP-ribose) polymerase 1. Like other members of the caspase family, caspase-3 minimally recognizes a five-amino-acid motif, usually located in a well-exposed loop within its substrates. Caspase-3 cleavage-site motif preferences have been systematically studied using peptides but not proteins. Here, we use a simple recombinant protein-based double brilliance bioluminescence resonance energy transfer (BRET2) biosensor assay for caspase-3 that enables robust and quantitative kinetic measurements in vitro. We used the biosensor by assessing its ability to distinguish between optimal and suboptimal cleavage-site motifs using a panel of BRET2 biosensors incorporating all 20 amino acids at the critical P4 position (the fourth residue N-terminal to the scissile bond). Except for arginine and lysine, we successfully determined the catalytic specificity (kcat/KM) for all other residues at P4. Notably, the range of proteolytic efficacies observed with BRET biosensors was significantly narrower than that previously reported using peptide-based libraries. Finally, we confirmed the biosensor's utility in apoptotic cells, demonstrating its robustness and broad applicability.","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13071377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430593","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

Bacterial pore-forming toxins: mechanisms and implications for host immunity. 细菌成孔毒素：对宿主免疫的机制和影响。

IF 4.5 3区生物学

Bioscience Reports Pub Date : 2026-03-23 DOI: 10.1042/BSR20250103

Kusum Lata, Shraddha Gandhi, Shamaita Chatterjee, Sindhoora Puravankara, Aakanksha Chauhan, Koyel Nandy, Kasturi Sarkar, Geetika, Gurvinder Kaur, Mandeep, Kausik Chattopadhyay

{"title":"Bacterial pore-forming toxins: mechanisms and implications for host immunity.","authors":"Kusum Lata, Shraddha Gandhi, Shamaita Chatterjee, Sindhoora Puravankara, Aakanksha Chauhan, Koyel Nandy, Kasturi Sarkar, Geetika, Gurvinder Kaur, Mandeep, Kausik Chattopadhyay","doi":"10.1042/BSR20250103","DOIUrl":"10.1042/BSR20250103","url":null,"abstract":"Pore-forming toxins (PFTs) are an ancient class of protein toxins specialized in membrane disruption and aiding in the pathogenicity of several different pathogens. These versatile toxins are multifunctional virulence factors that manipulate host signaling and immune responses and modulate the cellular fate. The pore-formation mechanism of PFTs proceeds in a stepwise manner, initiated by receptor binding, followed by oligomerization and membrane insertion. Beyond membrane disruption, PFTs trigger a cascade of immune signaling, inflammasome activation, and diverse cell death pathways such as apoptosis, pyroptosis, necroptosis, and ferroptosis. Additionally, there is increasing evidence suggesting that many PFTs undergo endocytosis and traffic to organelles such as mitochondria, lysosomes, the endoplasmic reticulum, and Golgi, where they modulate intracellular functions. Interestingly, some functions of PFTs are also independent of pore formation, highlighting the functional versatility of PFTs. Technological advancements ranging from cryo-electron microscopy and high-speed AFM to AI-guided modeling, single-molecule imaging, and membrane-mimetic systems have been central in providing structural and mechanistic insights into PFT biology. There has been the discovery of new toxins as well as new toxin families; many of them are antibacterial PFTs deployed in the microbial competition. The growing insights into PFT biology have opened new avenues for therapeutic innovation, both by developing strategies to neutralize PFT-mediated pathogenesis and by engineering PFTs for vaccine development and cancer treatment. In this review, we provide a comprehensive overview of PFT biology within the broader context of host-pathogen interactions and highlight the key structural, mechanistic, and cellular questions that remain unresolved.","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":"46 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13238964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147497596","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

Aminolevulinate inhibition of human coproporphyrinogen oxidase clarifies coproporphyrin III accumulation in porphyrias. 氨基乙酰丙酸抑制人卟啉原氧化酶澄清卟啉III在卟啉症中的积累。

IF 4.5 3区生物学

Bioscience Reports Pub Date : 2026-03-18 DOI: 10.1042/BSR20254015

Andreas Schedlbauer, Sarah Kratzwald, Margarita Gómez-Galán, Jon Gil-Martínez, Itxaso San Juan, Tania Pereira-Ortuzar, Fernando Lopitz-Otsoa, David Fernandez-Ramos, José M Mato, Oscar Millet

{"title":"Aminolevulinate inhibition of human coproporphyrinogen oxidase clarifies coproporphyrin III accumulation in porphyrias.","authors":"Andreas Schedlbauer, Sarah Kratzwald, Margarita Gómez-Galán, Jon Gil-Martínez, Itxaso San Juan, Tania Pereira-Ortuzar, Fernando Lopitz-Otsoa, David Fernandez-Ramos, José M Mato, Oscar Millet","doi":"10.1042/BSR20254015","DOIUrl":"10.1042/BSR20254015","url":null,"abstract":"Porphyrias are inherited or acquired disorders of heme biosynthesis characterized by heme deficiency and accumulation of toxic intermediates. In δ-aminolevulinic acid dehydratase deficiency porphyria (ALADP), patients consistently present elevated urinary δ-aminolevulinic acid (δ-ALA) and coproporphyrin III (COPRO III), yet the mechanistic basis of COPRO III accumulation remains unclear. This metabolic disturbance is also observed in the porphyria-like associated crises in hereditary tyrosinemia type I (HT1). Here, we investigated the effects of δ-ALA, COPRO III, and lead (Pb2+) on human coproporphyrinogen oxidase (CPOX), a key mitochondrial enzyme in heme biosynthesis. Using purified recombinant CPOX, we show that COPRO III binds with high affinity (KD ≈ 2.1 μM) and acts as a competitive inhibitor, while δ-ALA inhibits CPOX at millimolar concentrations through a non-competitive, likely covalent, mechanism. In vivo, δ-ALA accumulation in an HT1 mouse model led to hepatic COPRO III buildup, consistent with our in vitro findings and supporting a synergistic inhibition model in which δ-ALA promotes secondary COPRO III accumulation that further impairs CPOX. Additionally, Pb2+ was found to inactivate CPOX, likely through oxidative damage, providing a molecular explanation for enzyme dysfunction in porphyrin abnormalities in response to lead intoxication. Together, these results identify multiple metabolite- and toxin-dependent mechanisms that converge on CPOX inhibition, offering new insights into the pathophysiology of ALADP, among other porphyrias, lead intoxication, and HT1.","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13071380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146163866","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

Modulating Galectin-1 in human osteoblast-like cells alters mineralisation and influences the expression of genes associated with osteoblasts and osteocytes. 调节人成骨细胞样细胞中的半乳糖凝集素-1改变矿化并影响与成骨细胞和骨细胞相关的基因表达。

IF 4.5 3区生物学

Bioscience Reports Pub Date : 2026-03-18 DOI: 10.1042/BSR20253890

Amy C Ross, Lauren Feddersen, Jayesh Dudhia, Androniki Psifidi, Deborah J Guest

{"title":"Modulating Galectin-1 in human osteoblast-like cells alters mineralisation and influences the expression of genes associated with osteoblasts and osteocytes.","authors":"Amy C Ross, Lauren Feddersen, Jayesh Dudhia, Androniki Psifidi, Deborah J Guest","doi":"10.1042/BSR20253890","DOIUrl":"10.1042/BSR20253890","url":null,"abstract":"Bone formation, mineralisation, and remodelling are dependent on the activity of osteoblasts and osteoclasts. While many genes support bone development, their specific functions in the different stages of cell differentiation and maturation are often unknown. Galectin-1 (LGALS1) has roles in tumour angiogenesis and immune regulation but also enhances osteoblast differentiation of MSCs. The present study aimed to elucidate the role of LGALS1 in the osteogenesis of Saos2 cells. We demonstrated that Saos2 cells have a gene expression profile representing a mature osteoblast stage that shifts to an osteocyte-like profile under osteogenic conditions. We modulated LGALS1 using stable transfection to overexpress LGALS1 and lentiviral transduction of a short-hairpin RNA to knock down LGALS1. LGALS1 overexpression significantly reduced cell viability under basal culture conditions and significantly reduced mineralisation after 21 days of osteogenic culture. Knockdown of LGALS1 also significantly reduced cell viability under basal culture, but following osteogenic culture, a significant increase in mineralisation was observed. No effect on collagen deposition was seen following either knockdown or overexpression, suggesting that LGALS1 is involved in negatively regulating mineralisation. Osteogenic gene expression demonstrated few significant changes when LGALS1 was overexpressed. In contrast, knocking down LGALS1 resulted in many significant changes in osteogenic gene expression under both basal and osteogenic culture conditions. However, there was no clear correlation between the effect on gene expression and the increase in mineralisation. The present study demonstrated a novel role of LGALS1 in mature osteoblast-like cells. Further investigation into the regulatory pathways is warranted.","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13071376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146163954","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: Over-expression of microRNA-758 inhibited proliferation, migration, invasion and promoted apoptosis of non-small cell lung cancer cells by negatively regulating HMGB. 回撤：过表达microRNA-758通过负调控HMGB抑制非小细胞肺癌细胞的增殖、迁移、侵袭，促进细胞凋亡。

IF 4.5 3区生物学

Bioscience Reports Pub Date : 2026-02-28 DOI: 10.1042/BSR20180855_RET

Guo-Hua Zhou, Yi-Yu Lu, Jing-Lian Xie, Zi-Kun Gao, Xiao-Bo Wu, Wei-Shen Yao, Wei-Guang Gu

引用次数: 0

Retraction: Long non-coding RNA PVT1-mediated miR-543/SERPINI1 axis plays a key role in the regulatory mechanism of ovarian cancer. 缩稿：长链非编码RNA pvt1介导的miR-543/SERPINI1轴在卵巢癌的调控机制中起关键作用。

IF 4.5 3区生物学

Bioscience Reports Pub Date : 2026-02-18 DOI: 10.1042/BSR20200800_RET

Chong Qu, Chunmei Dai, Yahua Guo, Rui Qin, Junbao Liu

引用次数: 0

Retraction: The contribution of N2O3 to the cytotoxicity of the nitric oxide donor DETA/NO: an emerging role for S-nitrosylation. 撤回：N2O3对一氧化氮供体DETA/NO细胞毒性的贡献：s -亚硝基化的新作用。