Additional file 2 of SPP1 facilitates cell migration and invasion by targeting COL11A1 in lung adenocarcinoma

Additional file 2: Fig. S2. COL11A1 acts a tumor promotor of LUAD. A COL11A1 was positively associated with SPP1 in LUAD; B COL11A1 expression was significantly higher in LUAD tissues than normal tissues (*p <0.05, **p <0.01); C COL11A1 was significantly correlated to the TNM stage of LUAD; D patients with high COL11A1 expression had a poor OS than low COL11A1 patients

Additional file 1 of SPP1 facilitates cell migration and invasion by targeting COL11A1 in lung adenocarcinoma

Additional file 1: Fig. S1. Analysis of Sensitivity and publication bias in meta-analysis. A Sensitivity analysis of selected datasets. B A Begg’s funnel plot with 95% confidence limits

Additional file 3 of Comparative ribosome profiling reveals distinct translational landscapes of salt-sensitive and -tolerant rice

Additional file 3: Table S2. Differentially transcribed/translated genes under salt stress in seedling shoots of ‘Nipponbare’ (NB)

Additional file 1 of Comparative ribosome profiling reveals distinct translational landscapes of salt-sensitive and -tolerant rice

Additional file 1: Table S1. Raw data of rice RNA-seq and ribo-seq libraries

Image_2_JIP1 Deficiency Protects Retinal Ganglion Cells From Apoptosis in a Rotenone-Induced Injury Model.TIF

Retinal ganglion cells (RGCs) undergo apoptosis after injury. c-Jun N-terminal kinase (JNK)-interacting protein 1 (JIP1) is a scaffold protein that is relevant to JNK activation and a key molecule known to regulate neuronal apoptosis. However, the specific role of JIP1 in the apoptosis of RGCs is currently undefined. Here, we used JIP1 gene knockout (KO) mice to investigate the importance of JIP1-JNK signaling in the apoptosis of RGCs in a rotenone-induced injury model. In adult JIP1 KO mice, the number and electrophysiological functions of RGCs were not different from those of wild-type (WT) mice. Ablation of JIP1 attenuated the activation of JNK and the cleavage of caspase-3 in the retina after rotenone injury and contributed to a lower number of TUNEL-positive RGCs, a greater percentage of surviving RGCs, and a significant reduction in the electrophysiological functional loss of RGCs when compared to those in WT controls. We also found that JIP1 was located in the neurites of primary RGCs, but accumulated in soma in response to rotenone treatment. Moreover, the number of TUNEL-positive RGCs, the level of activation of JNK and the rate of cleavage of caspase-3 were reduced in primary JIP1-deficient RGCs after rotenone injury than in WT controls. Together, our results demonstrate that the JIP1-mediated activation of JNK contributes to the apoptosis of RGCs in a rotenone-induced injury model in vitro and in vivo, suggesting that JIP1 may be a potential therapeutic target for RGC degeneration.</p

Additional file 6 of Comparative ribosome profiling reveals distinct translational landscapes of salt-sensitive and -tolerant rice

Additional file 6: Table S5. Complete lists of gene ontology (GO) terms for genes translationally up- and down-regulated under salt stress in ‘Nipponbare’ (NB) or ‘Sea Rice 86’ (SR86)

Additional file 4 of Comparative ribosome profiling reveals distinct translational landscapes of salt-sensitive and -tolerant rice

Additional file 4: Table S3. Differentially transcribed/translated genes under salt stress in seedling shoots of ‘Sea Rice 86’ (SR86)

Additional file 2 of Comparative ribosome profiling reveals distinct translational landscapes of salt-sensitive and -tolerant rice

Additional file 2: Fig. S1 Ribosome profiles along 15–60% (W/V) sucrose gradients in ‘Nipponbare’ (NB) and ‘Sea Rice 86’ (SR86). (A-B) Profiles of ribosomes from NB under normal condition (0 h, A) or after 24-h salt stress (24 h, B). (C-D) Profiles of ribosomes from SR86 under normal condition (0 h, C) or after 24-h salt stress (24 h, D). Ribosome profiles are obtained by recording absorbance at 254 nm during sucrose gradient fractionation (from the top to the bottom of gradient). Fig. S2 Size distribution, periodicity and coverage on genomic elements of ribosome-protected mRNA fragments (RPFs) in ribo-seq libraries of ‘Nipponbare’ (NB) and ‘Sea Rice 86’ (SR86). (A) Size (in nucleotide, nt) distribution of RPFs in ribo-seq libraries of NB and SR86 under normal (0 h) and salt stress (24 h) conditions. (B) Periodicity (in Hz) analysis of RPFs in ribo-seq libraries of NB and SR86 under normal (0 h) and salt stress (24 h) conditions by the F-score test implemented in “Multitaper”, an R package. The horizontal dashed line indicates the cutoff for significant periodicity (P-value = 0.001) and the vertical dashed line shows the position of 1/3, the expected frequency (3-nt periodicity) of RPFs. (C) The percentage distribution of RPFs on exon, intron, 5′ UTR and 3′ UTR in the ribo-seq libraries of NB and SR86 under normal (0 h) and salt stress (24 h) conditions. “rep 1”, “rep 2” and “rep 3” represent the three biological repeats. Fig. S3 Metagene analysis of ribosome-protected mRNA fragments (RPFs) in ribo-seq libraries of ‘Nipponbare’ (NB) and ‘Sea Rice 86’ (SR86). (A-D) Metagene analysis of RPFs in ribo-seq libraries of NB under normal (0 h, repeat 2 for A and repeat 3 for B) and salt stress (24 h, repeat 2 for C and repeat 3 for D) conditions. (E-H) Metagene analysis of RPFs in ribo-seq libraries of SR86 under normal (0 h, repeat 2 for E and repeat 3 for F) and salt stress (24 h, repeat 2 for G and repeat 3 for H) conditions. Lines at positions of frame 0 (the main frame based on the annotated start codon), 1 and 2 are colored in purple, cyan and orange, respectively. Fig. S4 Clustering analysis of transcriptomic datasets from ‘Nipponbare’ (NB) and ‘Sea Rice 86’ (SR86). (A) Clustering analysis of transcriptomic datasets from NB under normal (0 h) and salt stress (24 h) conditions. (B) Clustering analysis of transcriptomic datasets from SR86 under normal (0 h) and salt stress (24 h) conditions. “rep 1”, “rep 2” and “rep 3” represent the three biological repeats. The color schemes indicate Euclidean distances between samples measured by DESeq2-normalized read counts. Fig. S5 Comparison of ribosome-protected mRNA fragment (RPF) distribution along gene coding sequences in ‘Nipponbare’ (NB) and ‘Sea Rice 86’ (SR86). (A-B) The coefficient of RPF depth of translationally up-regulated genes between normal (0 h) and salt stress (24 h) conditions (grey line) is compared to the expectation of complete concordance between the two conditions (orange line) in NB (A) and SR86 (B). (C-D) The coefficient of RPF depth of translationally down-regulated genes between normal (0 h) and salt stress (24 h) conditions (grey line) is compared to the expectation of complete concordance between the two conditions (orange line) in NB (C) and SR86 (D). The relative depth of RPFs displays as the mean of three biological repeats. Fig. S6 tRNA abundance in RNA-seq libraries of ‘Nipponbare’ (NB) and ‘Sea Rice 86’ (SR86). (A) tRNA abundance proxied by the percentage of reads mapped to each tRNA loci in NB and SR86 under normal (0 h) and salt stress (24 h) conditions. (B) The correlation between the strength of ribosome stalling and tRNA abundance

Image_1_JIP1 Deficiency Protects Retinal Ganglion Cells From Apoptosis in a Rotenone-Induced Injury Model.TIF

Retinal ganglion cells (RGCs) undergo apoptosis after injury. c-Jun N-terminal kinase (JNK)-interacting protein 1 (JIP1) is a scaffold protein that is relevant to JNK activation and a key molecule known to regulate neuronal apoptosis. However, the specific role of JIP1 in the apoptosis of RGCs is currently undefined. Here, we used JIP1 gene knockout (KO) mice to investigate the importance of JIP1-JNK signaling in the apoptosis of RGCs in a rotenone-induced injury model. In adult JIP1 KO mice, the number and electrophysiological functions of RGCs were not different from those of wild-type (WT) mice. Ablation of JIP1 attenuated the activation of JNK and the cleavage of caspase-3 in the retina after rotenone injury and contributed to a lower number of TUNEL-positive RGCs, a greater percentage of surviving RGCs, and a significant reduction in the electrophysiological functional loss of RGCs when compared to those in WT controls. We also found that JIP1 was located in the neurites of primary RGCs, but accumulated in soma in response to rotenone treatment. Moreover, the number of TUNEL-positive RGCs, the level of activation of JNK and the rate of cleavage of caspase-3 were reduced in primary JIP1-deficient RGCs after rotenone injury than in WT controls. Together, our results demonstrate that the JIP1-mediated activation of JNK contributes to the apoptosis of RGCs in a rotenone-induced injury model in vitro and in vivo, suggesting that JIP1 may be a potential therapeutic target for RGC degeneration.</p

Additional file 5 of Comparative ribosome profiling reveals distinct translational landscapes of salt-sensitive and -tolerant rice

Additional file 5: Table S4. Differentially translated genes under salt stress in seedling shoots of ‘Nipponbare’ (NB) or ‘Sea Rice 86’ (SR86)