Fig. 1. The conserved ClpB/DnaK bichaperone network resolves protein aggregates in mycobacteria. (A) Schematic of Mtb dnaK operon containing grpE, dnaJ1 and the regulator hspR. Another gene annotated as dnaJ2 is also present in the Mtb genome with the proposed regulator hrcA. ClpB is encoded by the gene Rv0384c. (B) Schematic of aggregated protein unfolding by the hexamer ClpB and refolding by DnaK with the assistance of the protein cofactors J proteins (DnaJs) and GrpE. DnaK and ClpB are ATPases. J proteins bring aggregated substrates to ClpB/DnaK and enhance ATP hydrolysis by DnaK. GrpE is a nucleotide exchange factor that stimulates release of ADP by DnaK. Small heat shock proteins (sHsps) are proposed to help solubilize aggregates for reactivation.

Fig. 3. Change in psychological well-being over acute treatment.

Fig 1. Dbr1 is a metallophosphoesterase.

Fig 1. Maps of BOLD functional MR imaging motor activation in a 59-year-old man with a GBM adjacent to the left PMC.

Fig.1 Proposed mechanism for MPL scavenging of TPO leading to neutropenia and thrombocytopenia in AML. PLTs, platelets.

Fig 3. Risk-adjusted survival of consensus clinical stage groups.

Fig 1. Graphical representation of BRCA1/2 heterozygous population frequencies in Exome Variant Server (EVS) and Exome Aggregation Consortium (ExAC) databases.

Fig 3. The Bcl2 family of proteins.

Fig 1. Mechanisms establishing CpG island methylator phenotype (CIMP) in colorectal cancer.

Fig 1. Lineage Tracing Systems Demonstrate Heterogeneity in TAM Ontogeny in Multiple Models of Glioma.

Fig 7. Apically Surfaced Cilia Can Ectopically Recruit Smoothened and Gli2 in the Absence of Agonist.

Fig 1. Computed tomography image of a patient with a horseshoe kidney.

Fig 1. Head and Neck Cancer Regions.

Fig 1. Rates of management for clinical stage I seminoma of the testis for the years 1998-2012 from hospitals with consistent reporting throughout all study years.

Fig 1. Relative position of infrarenal lumbar arteries (LA) and veins, right (R.) gonadal vein and inferior (Inf.) mesenteric artery.

Fig 1. Photomicrographs showing immunohistochemical staining of programmed death-ligand 1 (PD-L1; 22C3 antibody) in melanoma (MEL) samples.

Fig 8. Regions of BEST1 involved in Ca2+-dependent activation and ion selectivity.

Fig 1. First functional principal component (left column) and first functional partial least squares component (right column) for mucositis training (top row), dysphagia training (middle row), and dysphagia external validation (bottom row) data bootstrapped with 2000 replicates.

Fig. 1. Day 7 relationships to prostate necrosis. a, energy delivery.

Fig 1. Optical imaging of γ-emitters and photon beams.

Fig 1 Longitudinal high-frequency ultrasound image of level 6 metastatic papillary thyroid cancer node measuring 1.2 cm with microcalcifications and rounded appearance.

Fig 5. NTP donor specificity of the AfuTrl1 and CimTrl1 5′ kinase reaction.

Fig 4. miR-22 blocks rhabdomyosarcoma (RMS) tumor growth and dissemination.

Fig 4. The cysts of serous cystadenomas are lined by cuboidal cells, with round, central to slightly eccentric nuclei and clear cytoplasm (H&E, ×200).

Fig 1. Computed tomography (CT) images (a, b) before and (c) 15 d after one dose of nivolumab show an increase in pleural thickening.

Fig 1. Assay design.

Fig 4. Electrostatic interaction of α-amino group with conserved active site aspartate.

Fig 1. Lymph Node Organization and the Vascular–Stromal Compartment.

Fig 1. The interplay between the complement and the kinin generating systems on the endothelial cell (EC) surface.

Fig 1. 4D-CT: Axial and reformatted CT images of the neck over time to diagnose abnormal parathyroid tissue.

Fig 1. Schematic depicting structure of chimeric antigen receptors in largest published series to date.

Fig 1. Identical Differentiation Potential of PD iPSC and Control Lines.

Fig 2. N-Myc Overexpression Is Associated with Aggressive, NEPC-Like Prostate Cancer.

Fig 5. Preferential expression of Lgr5 in ventral ducts of the mammary gland during post-natal development, adulthood, and pregnancy.

Fig 5. Extramammary Paget disease.

Fig 1. Customized Sensing and Transcriptional Responses Using the synNotch Receptor in T Cells.

Fig 1. The PRINT Process.

Fig 9. Model that summarizes the proposed regulatory circuit that controls GBM phenotypes.

Fig 1. Individual Prediction Tools Included as Features in the REVEL Random Forest.

Fig 5. Optimization-based reconstructions fconv from the swine data with aortogram injection within a coronal slice specified by x  =  0.23 mm obtained with, respectively, parameter c  =  0.000, 0.025, 0.050, 0.075, 0.100, 0.200, 0.300 and 1.000, along with the reference reconstruction.

Fig 1.Fine-needle aspiration of lung.

Fig 1. A 52-year-old male with multiple HCCs.

Fig 2. Percent change in target lesion size from baseline for 47 evaluable patient.

Fig 1. Three folding states of pHLIP peptides in decreasing extracellular pH: unfolded and unbound peptide in solution (State I), unfolded peptide loosely interacting with the membrane lipid bilayer at physiological pH (State II), and folded peptide in α-helical conformation inserted across the membrane at low extracellular pH (State III).

Fig 1. Representative images of the longest diameters measured using calipers of a right cervical mass in (A) transverse plane, 2.6 cm and (B) coronal plane, 12.1 cm.

Fig 6. Short timescale modes of inhibition translate to long timescale proliferative response.

Fig 3. Predicted differences in quality-adjusted survival benefit by age, ER status, and family history of breast cancer.

Fig 6. Effect of PI3K inhibition on BCNP1 phosphorylation at serine residues.

Fig 1. PI3K/AKT/mTOR signaling is regulated by intrinsic feedback.

Fig 2. Diagram of the phosphatidylinositol 3-kinase signaling pathway.

Fig 1. Elevated [K+] within TIF silences the TCR-induced anti-tumour function of mouse and human T cells.

Fig 1. Metastatic landscape of the KPCY model.

Fig 1. Delay time (Tdelay) was optimized between start of 4D-CT acquisition and start of contrast injection.

Fig 3. Genomic Hallmarks of Thyroid Cancer along the Spectrum of Disease Progression.

Fig 1. Advanced imaging for high-content biopsy (HCBx) and molecular phenotyping.

Fig 5. Characterization of the response of mTOR-activating mutants to RAPTOR-mediated inhibition; mTOR kinase domain mutants exhibit increased kinase activity and display structural reorganization.

Fig 3. Fecal metabolites are altered by celecoxib in APCMin/+ and WT mice.

Fig 1. Schematic of next-generation sequencing and ctDNA analyses.

Fig 1. Spongiotic dermatitis.

Fig 1. Venn diagrams depicting number and percent of patients with local, lymph node (LN) and distant recurrence at first evidence of recurrence (A) or overall during follow-up. Seventeen patients (22%) did not recur during follow-up.

Fig 3. Stripped sequence libraries facilitate MS/MS analysis of large proteomes.

Fig 2. TANGO1 binding site located by X-ray crystallography.