TEFM facilitates transition from RNA synthesis to DNA synthesis at H-strand replication origin of mtDNA by Shigeru Matsuda, Masunari Nakayama, Yura Do, Takashi Ishiuchi, Mikako Yagi, Sjoerd Wanrooij, Kazuto Nakada, Fan-Yan Wei, Kenji Ichiyanagi, Hiroyuki Sasaki, Dongchon Kang, Takehiro Yasukawa

“…Herein, we examine the role of mitochondrial transcription elongation factor (TEFM) in this process. TEFM knockout results in decreased 7S DNA, strand-asynchronous replication intermediates, and mtDNA copy number, all of which are concordant with downregulation of RNA-to-DNA transition at OH. …”
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SOCS2 inhibits the tumorigenesis of GISTs and increases the sensitivity of GISTs to imatinib by suppression of KIT activation by Liangying Zhang, Kun Xiao, Shaoting Zhang, Sien Zhao, Zimei Liu, Ming Wang, Kaiyue Qin, Yuanyuan Yu, Shujing Li, Lijun Ma, Jianmin Sun

“…In KITV558A/WT mice, knockout of SOCS2 expression increased the tumorigenesis of GISTs and decreased the life span of the mice. …”
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Expression of MxA in esophageal cancer cell lines can influence sensitivity to chemotherapeutic agents but this does not require apoptosis by R. M. Hayes, T. R. O'Donovan, S. L. McKenna

“…We then evaluated siRNA knockdown of MxA in FLO‐1 cells and CRISPR knockout in OE21 cells. Knockdown of MxA significantly increased drug sensitivity and caspase‐3 activation in FLO‐1 cells. …”
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Mettl3-m6A-NPY axis governing neuron–microglia interaction regulates sleep amount of mice by Qihang Sun, Jinpiao Zhu, Xingsen Zhao, Xiaoli Huang, Wenzheng Qu, Xia Tang, Daqing Ma, Qiang Shu, Xuekun Li

“…We also showed that Mettl3 regulates neuropeptide Y (NPY) via m6A modification and Mettl3 conditional knockout (cKO) mice displayed significantly decreased expression of NPY in thalamus. …”
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Wogonin effects on the efflux transporters BCRP and MRP2, explain its effectiveness in ulcerative colitis: Implications for metabolic and transport interactions by Yuanyuan Liu, Zerong Zhang, Xiaoyan Li, Qinghong Hu, Zhangyu Jiang, Jia Lv, Jiayi Xue, Dongyu Wang, Jianxiong Cao, Lingyu Li, Xiaowen Ou, Lijun Zhu, Zhongqiu Liu, Tao Su

“…Moreover, in vitro results showed that after knockout of BCRP and MRP2, the concentration of wogonin increased, and its UGT metabolite wogonoside decreased in both cells and mitochondria. …”
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Maturation and detoxification of synphilin-1 inclusion bodies regulated by sphingolipids by Xiuling Cao, Xiang Wu, Lei Zhao, Ju Zheng, Xuejiao Jin, Xinxin Hao, Joris Winderickx, Shenkui Liu, Lihua Chen, Beidong Liu

“…Pharmacological inhibition of the sphingolipid metabolism pathway or knockout of its key genes results in a delayed IB maturation and increased SY1 cytotoxicity. …”
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MCU expression in hippocampal CA2 neurons modulates dendritic mitochondrial morphology and synaptic plasticity by Katy E. Pannoni, Quentin S. Fischer, Renesa Tarannum, Mikel L. Cawley, Mayd M. Alsalman, Nicole Acosta, Chisom Ezigbo, Daniela V. Gil, Logan A. Campbell, Shannon Farris

“…Using a CA2-specific MCU knockout (cKO) mouse, we found that MCU deletion impairs plasticity at distal dendrite synapses. …”
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NRBF2 plays a crucial role in the acquisition process of learning and memory, independent of the Vps34 complex by Songfen Wu, Songfen Wu, Songfen Wu, Haicai Zhuang, Haicai Zhuang, Haicai Zhuang, Xidan Zhou, Kuan Li, Kuan Li, Kuan Li

“…IntroductionNRBF2, a component of autophagy-associated PIK3C3/VPS34-containing phosphatidylinositol 3-kinase complex, plays a crucial role in learning and memory processes, yet its specific impact on memory and the underlying molecular mechanisms remains unclear.MethodsHere, we utilized NRBF2 knockout mice to examine its influence on the time course of fear memory. …”
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The guanine nucleotide exchange factor DOCK5 negatively regulates osteoblast differentiation and BMP2-induced bone regeneration via the MKK3/6 and p38 signaling pathways by Ju Ang Kim, Soomin Im, Jiwon Lim, Jung Min Hong, Hye Jung Ihn, Jong-Sup Bae, Jung-Eun Kim, Yong Chul Bae, Eui Kyun Park

“…C21 significantly enhanced osteoblast differentiation and mineral deposition in mouse MC3T3-E1 cells and in human and mouse BMSCs. Dock5 knockout (KO) mice exhibited increased bone mass and mineral apposition rate, with their BMSCs showing enhanced osteoblast differentiation. …”
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Erbin Regulates Tissue Factors Through Ras/Raf Pathway in Coagulation Disorders in Sepsis by Yang C, Lei C, Jing G, Xia Y, Zhou H, Wu D, Zuo J, Gong H, Wang X, Dong Y, Aidebaike D, Wu X, Song X

“…In vivo studies have shown that mice with Erbin deletion have more obvious enhanced coagulation function, and in vitro studies have shown that Erbin knockout mediated macrophage secretion of TF by activating the Ras/Raf pathway.Conclusion: Erbin reduces the coagulation activation by inhibiting TF release from macrophages.Keywords: Erbin, coagulation disorders, sepsis, tissue factor, macrophage…”
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A guide to selecting high-performing antibodies for Serine/threonine-protein phosphatase 2A 56 kDa regulatory subunit delta isoform (PPP2R5D) for use in Western Blot, immunoprecipi... by Carl Laflamme, Kathleen Southern, Riham Ayoubi, Maryam Fotouhi, Charles Alende

“…Here we have characterized six PPP2R5D commercial antibodies for Western Blot, immunoprecipitation, and immunofluorescence using a standardized experimental protocol based on comparing read-outs in knockout cell lines and isogenic parental controls. …”
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Exploring the functional role of POU5F1 using CRISPR RNP electroporation of zygote (CRISPR-EZ) in buffaloes by Meeti Punetha, Dharmendra Kumar, Suman Choudhary, Sheetal Saini, Kamlesh Kumari Bajwa, Surabhi Sharma, Manu Mangal, P. S. Yadav, T. K. Datta

“…We targeted the buffalo POU5F1 gene using the abovementioned parameters, which caused nonsense-mediated mRNA decay and led to complete knockout (KO) of the POU5F1 gene. We analyzed the mutation rates and mosaic mutations using tracking of Indels by decomposition (TIDE) software. …”
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Kaempferol protects against high-salt-induced hypertension and vascular endothelial injury by inhibiting ferroptosis through the ATF4/ACSL4 pathway by Qiuer Liang, Minghao Chen, Guangtian Chen, Pengli Xu, Lai Kwan Lam, Pengcheng Xie, Ting Xie, Wanqing Tu, Tianhao Liu, Xiaopeng Peng, Haoyao Yuan, Liguo Chen, Ya Xiao

“…Using an 8 % high-salt diet model, we evaluated the effects of Kae (200 mg/kg/day) in wild-type (WT) and activating transcription factor 4 (ATF4+/−) knockout mice. Additionally, human aortic endothelial cells (HAECs) cultured under high-salt conditions were used to assess Kae's protective effects, with ATF4 and acyl-CoA synthetase long-chain family member 4 (ACSL4) knocked down via siRNA transfection. …”
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Blockades of effector T cell senescence and exhaustion synergistically enhance antitumor immunity and immunotherapy by Xia Liu, Emily Shaw, Fusheng Si, Guangyong Peng, Yan Tao, Feiya Ma, David Bagley, Yuanqin Zhang

“…Loss-of-function strategies with pharmacological inhibitors and the knockout mouse model were used to identify the potential molecules and pathways involved in T cell senescence. …”
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The matricellular protein Fibulin-5 regulates β-cell proliferation in an autocrine/paracrine manner by Tomoko Okuyama, Takahiro Tsuno, Ryota Inoue, Setsuko Fukushima, Mayu Kyohara, Anzu Matsumura, Daisuke Miyashita, Kuniyuki Nishiyama, Yusuke Takano, Yu Togashi, Makiko Meguro-Horike, Shin-ichi Horike, Tatsuya Kin, A.M. James Shapiro, Hiromi Yanagisawa, Yasuo Terauchi, Jun Shirakawa

“…Fbln5 expression was increased upon glucose stimulation in β-cells of mouse and human islets. β-Cell-specific Fbln5-knockout (βFbln5KO) mice exhibit significantly reduced β-cell proliferation in vivo but not in vitro. …”
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NOX4 modulates breast cancer progression through cancer cell metabolic reprogramming and CD8+ T cell antitumor activity by Yingying Xiong, Yiming Weng, Shan Zhu, Jian Qin, Jia Feng, Xiaopeng Jing, Chao Luo, Wei Gong, Rui Sun, Min Peng

“…Although NADPH oxidase 4 (NOX4) has been implicated in various oncogenic processes, its exact function in breast cancer progression, metabolic reprogramming, and immune modulation remains unclear.MethodsWe used murine 4T1 and EO771 breast cancer models to generate NOX4 knockout (KO) cell lines via CRISPR/Cas9. In vitro assays (cell proliferation, colony formation, wound healing, and Seahorse metabolic analyses) and in vivo orthotopic tumor studies assessed the impact of NOX4 loss. …”
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O-GlcNAcylation attenuates ischemia-reperfusion-induced pulmonary epithelial cell ferroptosis via the Nrf2/G6PDH pathway by Liuqing Yang, Hexiao Tang, Jin Wang, Dawei Xu, Rui Xuan, Songping Xie, Pengfei Xu, Xinyi Li

“…Thus, we generated Ogt1-conditional knockout mice and found that Ogt1 deficiency aggravated ferroptosis, as evidenced by lipid reactive oxygen species (lipid ROS), malondialdehyde (MDA), Fe2+, as well as alterations in critical protein expression glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11). …”
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Genetic and pharmacological targeting of HINT2 promotes OXPHOS to alleviate inflammatory responses and cell necrosis in acute pancreatitis by Jiaqi Yao, Yuhong Jiang, Pengcheng Zhang, Yifan Miao, Xiajia Wu, Hang Lei, Zhijun Xie, Yong Tian, Xianlin Zhao, Juan Li, Lv Zhu, Meihua Wan, Wenfu Tang

“…Furthermore, CRISPR/Cas9-mediated HINT2 knockout significantly impaired the protective effects of Emo against AP-induced mitochondrial energy metabolism disorders, inflammatory responses, and acinar cell necrosis. …”
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The zinc receptor, ZnR/GPR39, modulates taste sensitivity by regulating ion secretion in mouse salivary gland by Moran Melamed, Hila Asraf, Noa Livne, Milos Bogdanovic, Anil Shendge, Gilad Shamir, Maayan Mero, Omer Adir, Avi Schroeder, Israel Sekler, Michal Hershfinkel

“…By monitoring transport of NH4+, a surrogate for K+, we revealed that Zn2+ upregulates the Na+/K+ ATPase pump activity in parotid and submandibular salivary gland epithelium from wildtype (WT), but not from ZnR/GPR39 knockout (KO), mice. Since Na+/K+ ATPase activity is crucial for solute transport, we compared saliva composition in WT and ZnR/GPR39 KO mice and found impaired ionic concentration and reduced saliva secretion in ZnR/GPR39 KO mice. …”
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Direct engulfment of synapses by overactivated microglia due to cadmium exposure and the protective role of Nrf2 by Siyao Li, Mingdan You, Chengjie Chen, Jingqi Fu, Yuanyuan Xu, Jingbo Pi, Yi Wang

“…Nrf2 is deeply implicated in the status of microglial activation; therefore, we also investigated whether it is involved in the above process. Nrf2 knockout mice and wild-type mice were used to explore prolonged Cd exposure-induced synaptic damages, learning-memory impairments, and microglial activation. …”
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