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  • 1.

    【2hr】Loss of desmoglein-2 promotes gallbladder carcinoma progression and resistance to EGFR-targeted therapy through Src kinase activation

    包量

    机译 通过SRC激酶活化促进衰减促进胆囊癌进展和抗EGFR靶向治疗的胆囊癌
    摘要：a Representative photomicrographs of immunohistochemical staining for EGFR in human tissues from patients with GBC. Scale bars: 100 μm. b The correlation between the EGFR expression pattern and survival rates in patients with GBC. Kaplan–Meier-based survival analysis for patients with membranous vs. cytoplasmic EGFR expression. c The isolation of GBC cells according to cell-surface EGFR expression using a FACSAria sorter, d cetuximab resistance in tumor cells with low EGFR expression. Cells expressing high or low levels of EGFR on the cell membrane were pretreated with 40 μg/ml cetuximab for 1 h, after which they were stimulated with 50 ng/ml of EGF for 48 h. Cell viabilities were assessed by MTT assays. *p < 0.05 compared with EGFR-high cells. e The expression levels of cell-junction cadherin proteins within EGFR-high and EGFR-low cell lysates were analyzed by western blotting using indicated antibodies. f Representative immunostaining of EGFR and Dsg2 in tissues of patients with GBC. Scale bars: 50 μm. g Western blot analysis of cytosolic and membrane protein fractions in shCtrl and shDsg2 cells. EGFR was dominantly expressed in the cytosolic fraction of both SNU308 shDsg2 and JCRB1033 shDsg2 cells.
  • 2.

    【2hr】Impaired RIPK1 ubiquitination sensitizes mice to TNF toxicity and inflammatory cell death

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    机译 受损的RIPK1泛素化使小鼠敏感至TNF毒性和炎症细胞死亡
    摘要：a Numbers of offspring at different embryonic days and adult age from intercrossing Ripk1K376R/+ mice. b Representative embryos of the Ripk1K376R/+ intercross at E12.5. Scale bars on the top left of each image indicate 2 mm. c Yolk sac of Ripk1+/+, Ripk1K376R/+ and Ripk1K376R/K376R intercross labeled for cleaved caspase-3 [green] and PECAM-1 [red] [scale bar 50 μm]. d Hematoxylin and eosin staining [upper panels, scale bar 100 μm] and IHC for cleaved caspase-3 [lower panels, scale bar 200 μm] of Ripk1+/+ and Ripk1K376R/K376R embryos. e IHC labeling for cleaved caspase-3 in the placenta labyrinths of Ripk1+/+ and Ripk1K376R/K376R embryos [scale bar 100 μm]. f Numbers of offspring from intercrossing Ripk1K115R/+ mice. g Histology of liver, spleen and small intestines of 12–15 months aged Ripk1+/+ and Ripk1K115R/K115R mice [scale bar 100 μm liver and small intestine, 200 μm spleen]. h Serum cytokine levels of IL-6 in Ripk1+/+ [n = 5] and Ripk1K115R/K115R [n = 5] 12–15 months old. i Survival of Ripk1+/+ in black [n = 13 males] and Ripk1K115R/K115R in red [n = 13 males] mice in TNF-induced SIRS model with 500 μg/kg TNF injected iv. Difference between the two groups by Mantel–Cox test: p = 0.0095.
  • 3.

    【2hr】Photoreceptor protection by mesenchymal stem cell transplantation identifies exosomal MiR-21 as a therapeutic for retinal degeneration

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    机译 间充质干细胞移植的光感受器保护鉴定外泌体miR-21作为视网膜变性的治疗方法
    摘要：A Schematic diagram demonstrating the study design of in vivo experiments on MNU-induced retinal degeneration. B Biodistribution of PKH26-labeled MSCs in the eye after intravitreal injection for 6 h. NC negative control, injection of MSCs without staining. Scale bar = 2.5 mm. C Tracing of PKH26-labeled MSCs (red) in the retina tissue counterstained by Hoechst 33342 (blue) after intravitreal injection for 24 h. MSCT mesenchymal stem cell transplantation after MNU injection, INL inner nuclear layer, ONL outer nuclear layer. Scale bar = 50 μm. Representative hematoxylin and eosin (H&E) staining images of retinal tissues (D) and the corresponding quantitative analysis of ONL thickness (E). Ctrl control, no MNU treatment, GCL ganglion cell layer, ONH optic nerve head. Scale bars = 50 μm. *P < 0.05 by the Kruskal–Wallis test for area under curve (AUC). N = 3 per group. Representative scotopic electroretinography (ERG) waveforms (F) and the corresponding quantitative analyses of amplitude changes of a-wave (G) and b-wave (H). *P < 0.05 by the Kruskal–Wallis tests. N = 6 per group. Representative photopic ERG waveforms (I) and the corresponding quantitative analysis of b-wave amplitude changes (J). *P < 0.05 by the Kruskal–Wallis tests. N = 6 per group. K Representative immunofluorescent (IF) staining images of retinal tissues showing cone photoreceptor bodies (white) counterstained by Hoechst 33342 (blue). Scale bars = 25 μm. Representative terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL, green) staining images of retinal tissues counterstained by Hoechst 33342 (blue) (L) and the corresponding quantitative analysis of percentages of TUNEL+ cells over total ONL cells (M). Scale bars = 50 μm. *P < 0.05 by the Kruskal–Wallis test. N = 6 per group. Representative flow cytometric images showing death of 661W cone photoreceptor cells (N) and the corresponding quantitative analysis of percentages of apoptotic (Annexin V+PI− plus Annexin V+PI+) 661W cells (O). The MSC group, Transwell co-culture of MNU-treated 661W cells with MSCs. PI propidium iodide. *P < 0.05 by the Kruskal–Wallis test. N = 3 per group. Data represent median ± range for (E) and (O). Data are represented as box (25th, 50th, and 75th percentiles) and whisker (range) plots for (G), (H), (J), and (M).
  • 4.

    【2hr】SPATA33 is an autophagy mediator for cargo selectivity in germline mitophagy

    包量

    机译 Spata33是一种用于种系细胞型货物选择性的自噬介质
    摘要：a Immunofluorescence of SPATA33 and ATG16L1 proteins in mouse testis. Anti-SPATA33, anti-ATG16L1 (Alexa Fluor®488), and TRITC-conjugated goat anti-rabbit IgG (H + L) antibodies were used to detect SPATA33 (red) and ATG16L1 (green). The nuclei were stained by Hoechst (blue). Images were taken by confocal fluorescence microscopy (SP8, Leica, Wetzlar, Germany). Positive signals were detected in Leydig cells (LC), Sertoli cells (Sn), spermatogonia (Sg), spermatocytes (Sc), and spermatids (Sp). Scale bar, 25 μm; scale bar in enlarged panels: 20 μm. b Cell sorting of spermatogonia (Sg), spermatocytes (Sc), and the round spermatids (Sp) from testis by cell flow sorter. Serial charts of cells were indicated. c Expression of Spata33 was detected in spermatogonia (Sg), spermatocyte (Sc), the round spermatids (Sp), and spermatozoa (sperm). The sperm cells were isolated from epididymis of adult mouse. RT-PCR was performed from mRNAs isolated from these cells. Actin was used as an internal control. d SPATA33 was colocalized with ATG16L1, LC3B, and VDAC2 in the mid-piece region (mitochondria region) of the sperm cells. The spermatozoa were extracted from epididymis of adult mice. The cells were stained with MitoTracker (mitochondria matrix marker, red). Immunofluorescence analysis were performed with anti-SPATA33, anti-ATG16L1 (Alexa Fluor®488), anti-VDAC2, anti-LC3B (Alexa Fluor®488), TRITC-conjugated goat anti-rabbit IgG (H + L), and FITC-conjugated rabbit anti-goat IgG (H + L) antibodies. The enlarged images were originated from the squares in the merged panels. The nuclei were stained by Hoechst (blue). Images were taken by confocal fluorescence microscopy (SP8, Leica). The graph on the right indicates sperm ultrastructure, highlighting cross-section of the mid-piece region, including axoneme, outer dense fiber, and mitochondrial sheath (red). Scale bar: 25 μm; scale bar in enlarged panels: 6 μm.
  • 5.

    【2hr】Cutting the molecular brakes to achieve cardiac regeneration

    包量

    机译 切割分子制动器以实现心脏再生
    摘要：Diverse sources elevate cytoplasmic Ctnnb1 in cardiomyocytes after infarction and can result in isoform switching by alternative splicing to raise levels of Pkm2 (typically in dimer but also monomer/tetramer forms) resulting in restricted Ctnnb1 mediated cytoprotection and cardiomyocyte induced proliferation, with direct or secondary effects on mitogenesis, angiogenesis and ATP-bioavailability to support the energy- and macromolecule-dependent hyperplasia (Akt; protein kinase-b; CamkII: calcium-dependent protein kinase II; Ctnnb1: beta-catenin-1; Dvl: dishevelled; Fak: focal adhesion kinase; Frzd: frizzled receptor; Glut-1/4: glucose transporter-1/4; Gsk-3β: glycogen synthase kinase 3-beta; Hif1α: Hypoxia-inducible factor 1-alpha; Ilk: integrin-linked kinases; Ldh: lactate dehydrogenase; Lrp5/6: low-density lipoprotein receptor-related protein; Nfat: Nuclear factor of activated T-cells; Nfkb: Nuclear factor NF-kappa-B; Nlk: nemo-like kinase; PEP: phosphoenolpyruvate; Pi3k: phosphoinositide 3-kinase; Pkc: protein kinase C; Pkm2: muscle pyruvate kinase 2; PPP: pentose phosphate pathway; Rapgef5: rap guanine nucleotide exchange factor 5; Ror: tyrosine-protein kinase transmembrane receptor; Tak1: transforming growth factor-β-activated kinase 1; Tcf/Lef: T-cell factor/lymphoid enhancer-binding factor).
  • 6.

    【2hr】Correction: Suppression of Patronin deficiency by altered Hippo signaling in

    包量

    机译 纠正：通过改变的河马信号传导抑制了审议缺乏
    摘要：Edited by E. Baehrecke
  • 7.

    【2hr】Correction: Loss of Ryanodine Receptor 2 impairs neuronal activity-dependent remodeling of dendritic spines and triggers compensatory neuronal hyperexcitability

    包量

    机译 校正：瑞尼诺受体2的损失损失树突刺的神经元活性依赖性重塑并触发补偿性神经元过度尺寸
    摘要：Edited by G. Melino
  • 8.

    【2hr】Building inner ears: recent advances and future challenges for in vitro organoid systems

    包量

    机译 建立内耳：最近的进步和体外有机体系统的未来挑战
    摘要：a Embryonic development of the inner ear (top) is mimicked in vitro to generate IEOs from PSCs (bottom) [21]. Top: during gastrulation of the blastula, neuroectoderm and non-neural ectoderm arises. Decreased TFGß expression and increased BMP and FGF signaling stimulate non-neural ectoderm formation. Within the non-neural ectoderm, the OEPD is formed due to diminished BMP expression, in addition to elevated FGF and WNT signaling levels. Continuing WNT activation as well as decreased FGF signaling gives rise to the otic placode within the OEPD. After invagination and formation of the otocyst, further patterning occurs by a combination of FGF, RA, WNT, and SHH signaling modulations, eventually giving rise to the inner ear. Bottom: PSCs are differentiated in a similar way, in which TFGß inhibition, together with FGF and BMP signaling activation, give rise to a non-neural ectoderm on the surface of the hPSC aggregate. With BMP inhibition and FGF signaling, the OEPD is formed in this surface ectoderm. Subsequent stimulation of WNT signaling gives rise to the otic placode within the OEPD. The placode invaginates to form otocysts that subsequently mature to IEOs. Other types of tissue, including cartilage and skin, are also induced within the aggregate. CNCC: cranial neural crest cells. b Schematic of the vestibular and cochlear cell types. Cell types described to be generated from hPSCs are colored. Ampulla: cross-section of one of the three ampullae of the semicircular canals as an example of the vestibular system. Vestibular hair cells in purple [21, 22, 24], supporting cells in aqua [15, 21–24], and neurons in red [12–14, 16, 19, 21–24] are described to be generated from hPSCs. The non-sensory cell types (in gray) are not described. Cochlea: a cross-section of the basal turn of the cochlea showing multiple cell types, with only neurons [12–14, 16, 19, 21–24], outer hair cells [22] and outer sulcus cells [20] reportedly generated from hPSCs. BLB: blood-labyrinth barrier, the barriers between the vasculature and inner ear fluids are present in both the vestibular system and cochlea, which have not been generated yet. Hair cells: Both type I [22] and type II [21, 24] vestibular hair cells, as well as outer cochlear hair cells are described [22]. Synaptic processes are also depicted [12, 13, 19, 21, 22].
  • 9.

    【2hr】Organoid systems to study the human female reproductive tract and pregnancy

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    机译 有机体系统研究人类女性生殖道和怀孕
    摘要：In vitro models of the human FRT used before the establishment of organoid systems.
  • 10.

    【2hr】Organoid-based modeling of intestinal development regeneration and repair

    包量

    机译 基于有机体的肠开发再生和修复模型
    摘要：Schematic organoid is depicted top left. Epithelial and mesenchymal cell types that constitute the stem cell niche are indicated [20–22, 24]. Green arrow represents cell migration from crypt to villus; red arrow represents repopulation of damaged epithelium from fetal-converted reserve stem cells. TA cell transit amplifying cell, ISC intestinal stem cell.
  • 11.

    【2hr】Neuronal cell life death and axonal degeneration as regulated by the BCL-2 family proteins

    包量

    机译 由BCl-2家族蛋白调节的神经元细胞寿命死亡和轴突变性
    摘要：In neuronal apoptosis it remains uncertain if PUMA activates BAX directly or indirectly. Unknown mechanisms are indicated by a “?”.
  • 12.

    【2hr】Defective endoplasmic reticulum-mitochondria contacts and bioenergetics in SEPN1-related myopathy

    包量

    机译 缺陷的内质网 - 线粒体触点和生物植物在Sepn1相关的肌病中
    摘要：Follow-up of body mass composition and calorimetric parameters between ages five (N = 12 mice per group) and 47 weeks (N = 6 mice per group). a Body weight; b percentage of fat mass and c lean mass over total body weight. Metabolic cage parameters during resting (day), activity (night), and average are shown: d food intake, e energy expenditure per kg of lean body mass, f energy balance corresponding to the difference between food intake and energy expenditure, g respiratory exchange ratio RER = 0.7 corresponding theoretically to 100% fatty acid oxidation, RER = 1 corresponding to 100% carbohydrate metabolism and h percentage of fatty acid oxidation in 5- and 32-week-old (w.o.) WT and SEPN1 KO.
  • 13.

    【2hr】Loss of p53 in mesenchymal stem cells promotes alteration of bone remodeling through negative regulation of osteoprotegerin

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    机译 间充质干细胞中P53的损失促进通过骨蛋白酶的负调节骨重塑的改变
    摘要：Representative images of microCT (a) and H&E staining (b) of bone from p53+/+, p53+/−, and p53−/− mice. Scale bar represents 100 µm, n = 5. Quantification of bone volume relative to total volume (c), trabecular bone thickness (d), and cortical bone thickness (e) from representative microCT scans in a, n = 5. Serum OPG (f) and RANKL (g) were measured in p53−/− (n = 6), p53+/− (n = 6), p53+/+ (n = 6) mice. h RANKL/OPG ratio was calculated according the serum values of OPG and RANKL obtained in f and g. i, j Overall survival of prostate cancer patients was analyzed by Synergy2G. {"type":"entrez-geo","attrs":{"text":"GSE16560","term_id":"16560"}}GSE16560 was selected. 30 samples from batch 6 (i) and 64 samples from batch 4 (j) were shown as plots. OPGhighTP53low or OPGlowTP53high were shown as blue, and the others were shown as red. Data are presented as mean ± SD. *p < 0.05, **p < 0.01, n.s. not significant. All replicates are biological replicates.
  • 14.

    【2hr】Yolk sac-derived Pdcd11-positive cells modulate zebrafish microglia differentiation through the NF-κB-Tgfβ1 pathway

    包量

    机译 yolk Sac衍生的PDCD11阳性细胞通过NF-κB-TGFβ1途径调节斑马鱼微胶质细胞分化
    摘要：a Schematic diagram showing the two major function domains of PDCD11: N-terminal Ribosome domain (1–1407) and C-Terminal Coil domain (1408–1871). b Gross morphology of 3 dpf WT and pdcd11 mutants. c qPCR confirmation of hyperactivated inflammatory pathway genes, including tnfa, il1b, and il6, in 22 hpf pdcd11 mutants, which could not be restored by combined p53 mutation. d–eIl6 and il1b expression in the brain of WT or pdcd11 mutants with p53 mutated or not examined by WISH at 52 hpf. f WISH analysis of l-plastin, mfap4, and csf1ra expression in 24 hpf WT and pdcd11 mutant embryos. Red arrows indicate csf1ra-positive cells in the brain. g Microglia development in 3 dpf WT and pdcd11 mutants by WISH assessment of apoeb and Neutral Red staining. hL-plastin and mfap4 expression pattern in 3 dpf WT and pdcd11 mutants. i Morphology of macrophages in the brain and caudal hematopoietic tissue (CHT) were examined using the Tg(mpeg1:GFP) transgenic line. White arrows indicate the vacuolated macrophages found in the pdcd11 mutant. j Increased tnfa mRNA expression in sorted macrophages Tg(mpeg1:GFP) from 60 hpf pdcd11 mutants as compared with WT controls. k qPCR examination of the expression of macrophage-related genes cxcr3.1 and cxcr3.2 in 22 hpf WT and pdcd11 mutants. l WISH analysis of cxcr3.1 and cxcr3.2 expression in 22 hpf WT and pdcd11 mutants. The number positioned in the lower right corner of d–h, l represent the number of zebrafish embryos shown positive phenotypes versus the total number of embryos examined. Scale bar: 100 μm. Black horizontal lines indicate mean ± standard error of mean (SEM). Means ± SEM are shown for three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001 (Student’s t test).
  • 15.

    【2hr】Intranasal delivery of mesenchymal stem cell secretome repairs the brain of Alzheimer’s mice

    包量

    机译 间充质干细胞沉淀的鼻内递送修复阿尔茨海默氏症老鼠的脑
    摘要：a Experimental design. b Comparison of the discrimination index (DI) of APP/PS1 mice and their age-matched WT littermates receiving either PBS, MSC-CS or MSC-UCS and tested in the NORT. DI of WT and APP/PS1 mice treated with PBS or MSC-CS and tested in the NORT 7 days (c) and 14 days (d) post-injection. Data are expressed as scatter plots with mean ± SEM. One-way ANOVA in b and d. Two-way ANOVA in c, *P < 0.05; **P < 0.01 Tukey’s multiple comparison post-hoc test.
  • 16.

    【2hr】RIP3-mediated necroptosis is regulated by inter-filament assembly of RIP homotypic interaction motif

    包量

    机译 RIP3介导的肮脏衰竭由裂纹偶开型相互作用基序的灯丝组件调节
    摘要：a Schematic representation of full-length M45 and M45 (1–292 aa) with or without RHIM mutations used in these studies (left). Schematic representation of M45 truncations with tandem FKBPv domain at its C-terminus (right). The four conserved residues (IQIG of M45) of RHIM or their alanine mutations destroy RHIM function are indicated. b Cell necroptosis is blocked by full-length or N-terminal portion of M45. The cells with indicated lentivirus infection were treated with T/S/Z for human HT-29 for 10 h. The number of surviving cells was determined by measuring ATP levels using CellTiter-Glo kit (lower). The data are represented as the mean ± standard deviation (SD) of duplicate wells. Similar results were obtained from at least three independent experiments. T TNF-a, S Smac mimetic, Z z-VAD. The final concentrations of 10 ng/ml TNF-a, 100 nM Smac mimetic, and 20 μm z-VAD were used. Identical concentrations of these necrosis-inducing agents were used in subsequent experiments unless otherwise stated. The untreated cells were harvested and whole-cell extracts were prepared and normalized to the same concentration. Aliquots of 20 μg whole-cell lysates were subjected to SDS-PAGE followed by western blot analysis of M45 (Myc) and β-Actin which is shown as a loading control (upper). c Mapping the M45 functional region. HT-29 cells were infected with lentiviruses encoding M45 truncations treated with T/S/Z for the indicated time. The number of surviving cells was determined by measuring ATP levels (lower). The expression level of M45 truncations was measured by western blot analysis (upper). Statistical significance was determined using two-way ANOVA followed by a Dunnett post hoc test. Significance between samples is indicated in the figures as follows: ns not significant; *P < 0.05, **P < 0.01, and ***P < 0.001. d The chimaeric M45 containing ICP6 or RIP3–RHIM could barely block TNF-induced cell necrosis. The schematic diagram of chimaeric M45 is shown in Fig. S1A. HT-29 cells with indicated lentivirus infection were treated with T/S/Z for 10 h. The number of surviving cells was determined by measuring ATP levels (lower). The data are represented as the mean ± SD of duplicate wells. The expression level of chimaeric M45 was measured by western blot analysis (upper).
  • 17.

    【2hr】Phosphorylation by Aurora B kinase regulates caspase-2 activity and function

    包量

    机译 Aurora B激酶的磷酸化调节Caspase-2活性和功能
    摘要：a Schematic diagram of phosphorylation site analysis of caspase-2. b Caspase-2 phosphorylation sites identified by LC–MS/MS. The phosphorylated amino acid position, charge, mass error, peptide location in caspase-2, phosphorylated S/T site position in caspase-2 and localisation probability are indicated. Phosphorylated residues are indicated in brackets. Spectra for the peptides in (b) can be found in Supplementary Fig. S2. c Phosphorylation sites in caspase-2 identified by mass spectrometry. Functionally reported sites are indicated in red. S (Ser) or T (Thr) (in black) indicates positions of novel potential phosphorylation sites. NLS nuclear localisation signal. C320 catalytic Cys. d Multiple amino acid sequence alignment showing conservation of phosphorylation sites in caspase-2 from different species. Newly identified and known phosphorylation sites with high homology are shaded in purple and grey, respectively.
  • 18.

    【2hr】Aquaporin 1 promotes sensitivity of anthracycline chemotherapy in breast cancer by inhibiting β-catenin degradation to enhance TopoIIα activity

    包量

    机译 Aquaporin 1通过抑制β-catenin降解来增强TopoIiα活性促进蒽环类化疗的敏感性。
    摘要：a The Venn diagram showed DEGs in breast cancer tissues and their paired adjacent tissues. DEGs in EPI sensitive group and non-sensitive group, along with 103 overlapped DEGs were also shown. Genes with P < 0.05 and |fold change| > 2 were considered as DEGs. b The volcano plot: green, red, and black points represented downregulated (n = 105), upregulated (n = 185), and no statistically significant difference genes, respectively, in the EPI non-sensitive group versus the EPI sensitive group. X-axes showed log2 (fold change) and y-axes showed −log10 (P value). c The heatmap and cluster analysis: EPI non-sensitive group: blue, EPI sensitive group: pink. Red denoted high expression and green represented low expression. The high expression of AQP1 in EPI sensitive group was shown. Not all DEGs in the figure were labeled. d OS (left panel) and PFS (right panel) curves of IDC patients treated with CEF-based therapies (upper panel) or non-CEF-based therapies (lower panel) with AQP1 expression (log-rank test). e OS (left panel) and PFS (right panel) curves of patients with high expression of AQP1 (upper panel) or low expression of AQP1 (lower panel) who received CEF-based therapies or non-CEF-based therapies (log-rank test). f OS (left panel) and PFS (right panel) curves of IDC patients treated with CMF-based therapies with AQP1 expression (log-rank test). g OS (left panel) and PFS (right panel) curves of patients with high expression of AQP1 (upper panel) or low expression of AQP1 (lower panel) who received CEF-based therapies or CMF-based therapies (log-rank test). h Representative immunohistochemical images of AQP1 expression in the EPI non-sensitive group (n = 37) and the EPI sensitive group (n = 33), respectively. Scale bars: 100 μm, (left panel). The AQP1 expression was higher in the EPI sensitive group than the EPI non-sensitive group (Mann–Whitney U test, P = 0.0378; right panel).
  • 19.

    【2hr】Cell fate determined by the activation balance between PKR and SPHK1

    包量

    机译 通过PKR和SPHK1之间的激活平衡确定的单元格命运
    摘要：a The levels of phosphorylated PKR and SPHK1 were evaluated following treatment with 2 μM or 400 nM DON for the indicated time periods in HepG2 and HEK293T cells. The cells were then harvested and subjected to western blotting analysis. The dosages of DON administrated in both cells are chosen according to IC50 measurements by CCK-8 assay as shown in Supplementary Fig. 1. b The levels of phosphorylated PKR and SPHK1 were evaluated following irradiation with UVC for 10 min, treatment with 10 ng/mL TNF-α, or treatment with 1 μg/mL LPS for 3 h in HepG2 and HEK293T cells. The cells were then harvested and subjected to western blotting analysis. c The expression of ER stress-related proteins were evaluated during PKR overexpression and PolyI:C administration. HEK293T cells were transfected with pCDNA3.1–PKR or pCDNA3.1 for 24 h or treated with 10 μg/mL PolyI:C for 3 h. The optimization of PolyI:C concentrations as the positive control is shown in Supplementary Fig. 5. The cells were then harvested and subjected to western blotting analysis. d, e ER stress-related protein levels during DON or TNF-α exposure were evaluated in PKR knockout cells. HEK293T control and PKR knockout cells at 70% confluence were incubated with 400 nM DON or 10 ng/mL TNF-α for 3 h. The cells were then harvested and subjected to western blotting analysis. f Cytotoxicity of DON was evaluated in PKR knockout cells. HEK293T control and PKR knockout cells at 70% confluence were treated with various concentrations of DON for 24 h. Cell viability was then determined with CCK-8 (n = 6). g Cell apoptosis resulting from TNF-α treatment in PKR knockout cells. HEK293T control and PKR knockout cells were evaluated with 10 ng/mL TNF-α by targeting cleaved caspase 9. The cells were then harvested and subjected to western blotting analysis. h The expression levels of IKKα and phosphorylated MAPKs during SPHK1 overexpression. HepG2 cells were transfected with pCDNA3.1–SPHK1 or pCDNA3.1 for 24 h. The cells were then harvested and subjected to western blotting analysis. i, j The expression levels of DON- and UV-induced IKKα and phosphorylated MAPKs were evaluated in shSPHK1 cells. HepG2 shLacZ and shSPHK1 cells at 70% confluence were incubated with 2 μM DON for 3 h or exposed to UVC irradiation for 10 min. The cells were then harvested and subjected to western blotting analysis. k Cytotoxicity of DON in shSPHK1 cells. HepG2 shLacZ and shSPHK1 cells at 70% confluence were treated with various concentrations of DON for 24 h. Cell viability was then determined with CCK-8 (n = 6). l Cell apoptosis resulting from TNF-α treatment in shSPHK1 cells. HepG2 shLacZ and shSPHK1 cells were evaluated with 10 ng/mL TNF-α by flow cytometry. The data were analyzed using FlowJo software. The results are the means ± SEMs of at least three independent experiments. Statistical significance was defined as *p < 0.05, **p < 0.01, or ***p < 0.001.
  • 20.

    【2hr】Correction: Protein phosphatase 6 is a key factor regulating spermatogenesis

    包量

    机译 校正：蛋白质磷酸酶6是调节精子发生的关键因素
    摘要：Edited by H.-U. Simon
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