BUSCADOR RECOLECTA

Figure S1. Images of whole gel western blots and protein markers Table S1. Primers used for qPCR amplification Table S2. Mass spectrometry-driven proteomics analysis allowed the identification of a total of 279 proteins with high confidence Table S3. Proteins included in clusters 1 and 2 in Figure 4C, Peer reviewed

Appendix A. Supplementary materials: Supplementary Data S1. Supplementary Raw Research Data., Peer reviewed

Resources available on the publisher's site: http://dx.doi.org/10.1093/cvr/cvab127, Peer reviewed

Additional file 1: Fig. S1. Characterization of rice plants grown under different Fe conditions. Fig. S2. Venn diagrams representing transcriptional changes in response to M. oryzae infection in leaves of High-Fe and Control plants. Fig. S3. GO enrichment analysis of genes down-regulated by M. oryzae infection in Control and High-Fe plants (48 hpi). Fig. S4. Hierarchical clustering of differentially expressed genes by RNA-Seq analysis. Fig. S5. Phenylpropanoid biosynthesis pathway. Genes whose expression is regulated by M. oryzae infection are indicated. Fig. S6. Expression of diterpene phytoalexin biosynthetic genes in leaves of Control and High-Fe plants (−, mock-inoculated; +, M. oryzae- inoculated). Fig. S7. Accumulation of phytoalexins in leaves of Control and Low-Fe plants. Fig. S8. Expression of genes involved in Fe homeostasis in leaves of Control and High-Fe plants (−, mock-inoculated; +, M. oryzae- inoculated). Fig. S9. Malate dehydrogenase (MDH) assay in total protein extracts and apoplast fluid from Control and High-Fe plants (mock-inoculated and M. oryzae- inoculated). Fig. S10. Trypan blue staining for cell death in M. oryzae-infected leaves of Control and High-Fe rice plants. Fig. S11. Accumulation of Fe in sheaths of Low-Fe, Control-Fe, and High-Fe in rice plants that have been treated with the ferroptosis inhibitor Ferrostatin-1 (+ Fer-1), or not (− Fer-1)., Consejo Superior de Investigaciones Cientificas (CSIC), Peer reviewed

1 table., Additional file 2: Table S1. Differentially expressed genes (DEGs) in leaves of High-Fe plants relative to Control plants identified by RNASeq analysis (no infection conditions)., Peer reviewed

File Name: Supplementary Data 1 Description: List of differentially regulated genes with statistically significant difference between WT and Vav3–/– B‐cell progenitors File Name: Supplementary Data 2 Description: Gene‐ontology (molecular functions, biological function and pathway) analyses of all the differentially expressed genes in Vav3 deficient p190 BCR‐ABL+ B‐cell progenitors. File Name: Supplementary Data 3 Description: Exome sequencing and evaluation of mutations and/or deletion in genes known to be mutated and/or deleted in B‐ALL. File Name: Supplementary Data 4 Description: Differentially bound peaks identified by Diffbind analyses of Bmi1 CUT&RUNseq data. File Name: Supplementary Data 5 Description: Differentially bound peaks identified by Diffbind analyses of Ring1b CUT&RUNseq data File Name: Supplementary Data 6 Description: Differentially bound peaks identified by Diffbind analyses of H2AK119Ub CUT&RUNseq data. File Name: Supplementary Data 7 Description: Overlapping genes with decreased Bmi1, Ring1b and H2AK119Ub occupancy in Vav3−− leukemic B‐cell progenitors. File Name: Supplementary Data 8 Description: Overlapping genes with increased Bmi1, Ring1b and H2AK119Ub occupancy in Vav3−− leukemic B‐cell progenitors., Peer reviewed

TABLE S1. Baseline clinical characteristics of patients that underwent abdominal surgery. From these patients, abdominal adipose tissue was obtained, and a vascular study was also performed. Table S2. Baseline clinical characteristics of patients that underwent open surgery for abdominal aortic aneurysm repair. From these patients, aortic perivascular adipose tissue was obtained. Table S3. RT-PCR primers and probes. Table S4. Effect of high fat diet (HFD) on perirenal and abdominal fat and adiposity in male and female mPGES-1+/+ and mPGES-1−/− mice. Table S5. Effect of high fat diet (HFD) on systolic blood pressure (SBP) levels in male and female mPGES-1+/+ and mPGES-1−/− mice. Figure S1. mPGES-1 expression and PGE2 production is unchanged in different tissues from control and obese mice. (A) mRNA levels of Ptges in white abdominal adipose tissue (WAT), perivascular adipose tissue (PVAT), aorta and heart of C57BL/6 J mice treated with normal diet (control) or high fat diet (HFD). PGE2 production in aorta (B) and heart (C) of each experimental group. In all bar graphs, each dot represents one mouse. Data represent mean ± SEM. The number of animals in each group is shown below each bar. Figure S2. mPGES-1 deficiency protects against high fat diet (HFD)-induced aortic insulin resistance. Concentration-response curves to insulin of aorta from mPGES-1+/+ (A) and mPGES-1−/− (B) mice fed with normal (control) and HFD. Data represent mean ± SEM. *p < .05 vs control by two-way ANOVA. The number of animals in each group is shown in parentheses. Figure S3. mPGES-1 deficiency partially prevents extracellular matrix deposition in perivascular adipose tissue (PVAT) but not in aorta or mesenteric arteries. (A) Quantification and representative images of Sirius Red-stained aortas and (B) mRNA levels of Tgfb in aorta from mPGES-1+/+ and mPGES-1−/− mice fed with normal diet (control) and HFD. mRNA levels of Fn1 (C), Tgfb (D) and Ctgf (E) from PVAT from all the experimental groups. (F) Representative images and quantification of 3D elastin structure in the internal elastic lamina of mesenteric resistance arteries (MRA) from all the experimental groups. Image size: 61.9x61.9 μm. In all bar graphs, each dot represents one mouse. Data represent mean ± SEM. *p < .05 vs control of each genotype. +p < .05 vs mPGES-1+/+ under the same diet, by one-way ANOVA or non-parametric Kruskal-Wallis test. The number of animals in each group is shown below each bar. Figure S4. mPGES-1 deficiency does not modify oxidative stress of inflammatory markers in the heart. (A) mRNA levels of Cybb, Nox4, Il1b and IL6 from hearts from mPGES-1+/+ and mPGES-1−/− mice fed with normal diet (control) and high fat diet (HFD). (B) Malondialdehyde (MDA) levels in heart homogenates of each experimental group. In all bar graphs, each dot represents one mouse. Data represent mean ± SEM. The number of animals in each group is shown below each bar. Figure S5. mPGES-1 deficiency protects against high fat diet (HFD)-induced body weight gain in female mice. (A) Body weight gain, (B) basal glucose levels, (C) glucose tolerance test (GTT), (D) area under the curve of GTT and (E-F) insulin tolerance test (ITT) in female mPGES-1+/+ and mPGES-1−/− mice fed with normal diet (control) and HFD. In bar graphs, each dot represents one replicate. Data represent mean ± SEM. *p < .05 vs control of each genotype. +p < .05 vs mPGES-1+/+ HFD by one-way or two-way ANOVA or non-parametric Kruskal-Wallis test. The number of animals in each group is shown in parentheses or below each bar. Figure S6. mPGES-1 deficiency protects against high fat diet (HFD)-induced mesenteric resistance arteries endothelial dysfunction in female mice. Concentration-response curves to acetylcholine (ACh) and diethylamine NONOate (DEA-NO) of aorta (A-D) and mesenteric resistance arteries (MRA) (E-H) from female mPGES-1+/+ and mPGES-1−/− mice fed with normal (control) and HFD. Data represent mean ± SEM. *p < .05 vs control by two-way ANOVA. The number of animals in each group is shown in parentheses. Figure S7. mPGES-1 deficiency does not affect aortic insulin vasodilation or cardiac structure in female mice. (A-B) Concentration-response curves to insulin of aorta from mPGES-1+/+ (A) and mPGES-1−/− (B) female mice fed with normal (control) and high fat diet (HFD). (C) Left ventricle (LV) weight normalized to tibia length (TL) from all experimental groups. In bar graphs, each dot represents one replicate. Data represent mean ± SEM. *p < .05 vs control of each genotype by one-way or two-way ANOVA or non-parametric Kruskal-Wallis test. The number of animals in each group is shown in parentheses or below each bar., Peer reviewed

1 table., Additional file 3: Table S2. List of differentially expressed genes (DEGs) in leaves of High-Fe (S2a) and Control (S2b) plants at 48 hpi with M. oryzae spores, relative to the corresponding mock-inoculated plants., Consejo Superior de Investigaciones Cientificas (CSIC), Peer reviewed

1 table., Additional file 4: Table S3. GO enrichment analysis of genes regulated by M.oryzae infection in High-Fe and Control plants relative to the corresponding mock-inoculated plants., Consejo Superior de Investigaciones Cientificas (CSIC), Peer reviewed

Material complementario S1 . Resultado del carcinoma cutáneo de células escamosas con enfermedad residual microscópica. Figura S1 . Diagrama de flujo de selección de muestras. Figura S2 . Curvas de Kaplan-Meier para los eventos de desenlace en función de la afectación del margen profundo tras la cirugía. Tabla S1 . Datos descriptivos de la cohorte de pacientes con carcinoma cutáneo de células escamosas (CSCC) con enfermedad residual microscópica (MRD) después de la cirugía. Tabla S2 . Resultado según el tipo de margen afectado. Tabla S3 . Utilidad de la radioterapia postoperatoria ajustada por estadio T. Tabla S4 . Análisis univariado y modelos multivariados para la utilidad de PORT en CSCC con MRD (modelos basados ​​en sistemas de estadificación)., Peer reviewed