Association of EAT, VAT and subclinical atherosclerosis.

<p>Association of EAT, VAT and subclinical atherosclerosis.</p

Characteristics of the study population.

<p>Characteristics of the study population.</p

Pearson's correlation between regional fat depots.

<p>Pearson's correlation between regional fat depots.</p

Additional file 2: of Functional genomics identifies specific vulnerabilities in PTEN-deficient breast cancer

Figure S1. PTEN protein abundance of breast cancer cell lines. (A) Western blots showing PTEN and actin (loading control) abundance in 19 breast cancer cell lines. (B) Scatter plot of RPPA-measured PTEN abundance reported by Marcotte et al. [17] versus PTEN abundance that we quantified through densitometric analysis of western blot bands in (A). Cell lines were categorized as PTEN-expressing (in black) or PTEN-deficient (in red) based on PTEN protein abundance. (PNG 201 kb

Additional file 1: of Cenani-Lenz syndactyly syndrome - a case report of a family with isolated syndactyly

Table S1. Variant data – Data related to Whole Exome Sequencing (WES). (XLSX 274 kb

Additional file 1: of Functional genomics identifies specific vulnerabilities in PTEN-deficient breast cancer

Table S1. Growth media for breast cancer cell lines used in study. Table S2. PTEN protein abundance in cell lines quantified by western blot. Table S3. Classification of breast cancer cell lines as PTEN+ or PTEN- based on PTEN protein abundance. Table S4. Primary screen results and hits. Table S5. Details of shRNA library used in secondary screen. Table S6. shRNA barcode counts from secondary screen in 11 cell lines. Table S7. Fold-change in shRNA barcode count for 11 cell lines. Table S8. shRNAs used in ATARiS gene solutions, with ATARiS consistency scores per shRNA. Table S9. ATARiS gene level scores for 11 cell lines. Table S10. Secondary screen results and hits. Table S11. Screen results (zGARP scores) from Breast Functional Genomics Dataset. Table S12. Screen results (DEMETER scores) from Cancer Dependency Map Dataset. Table S13. Screen results (z scores) from Kinase Dependency Profiles Dataset. (XLSX 22688 kb

The use of cognitive-behavioural therapy in occupational therapy of eating disorders.

Additional file 2: Table S2. SPN genotypes flanking the p.G120C mutation present in the fetus and 13 unaffected relatives

MOESM7 of A novel ICK mutation causes ciliary disruption and lethal endocrine-cerebro-osteodysplasia syndrome

Additional file 7: Figure S5. Ciliary length is not markedly altered in ECO patient-derived fibroblasts

MOESM4 of A novel ICK mutation causes ciliary disruption and lethal endocrine-cerebro-osteodysplasia syndrome

Additional file 4: Figure S2. Alignment of the protein kinase domain in ICK, MAK and MOK in different species

MOESM3 of A novel ICK mutation causes ciliary disruption and lethal endocrine-cerebro-osteodysplasia syndrome

Additional file 3: Figure S1. The ICK missense mutation (c.358G > T; p.G120C) segregates with disease