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Fig. 1 in Deciphering the roles of leucine-rich repeat receptor-like protein kinases (LRR-RLKs) in response to Fusarium wilt in the Vernicia fordii (Tung tree)

Fig. 1. The maximum likelihood tree and synteny analysis among these five Euphorbiaceae genomes. All LRR-RLKs were divided into 22 groups and were distinguished by different colors. These different groups were determined and defined based on the A. thaliana homologs nomenclature within the same group (Shiu and Bleecker, 2001b). The synteny relationships between different Euphorbiaceae genomes were represented by different links. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

opennotspecifiedMay 2021View details →

Fig. 2 in Deciphering the roles of leucine-rich repeat receptor-like protein kinases (LRR-RLKs) in response to Fusarium wilt in the Vernicia fordii (Tung tree)

Fig. 2. The circos figures for chromosome locations with segmental duplication links in M. esculenta (Me; green), H. brasiliensis (Hb; orange), J. curcas (Jc; yellow), R. communis (Rc; blue), and V. fordii (Vf; cyan). The different lines suggested segmented duplicated gene pairs among these five Euphorbiaceae genomes. All the collinearity pairs are represented by grey background. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Fig. 8 in Mutagenesis of a Lotus japonicus GSK3β/Shaggy-like kinase reveals functionally conserved regulatory residues

Fig. 8. Effect of overexpression of different LjSK1 variants in L. japonicus hairy roots. Physiological parameters of L. japonicus wild type hairy roots transformed with LjSK1 variants: LjSK1 90–467 lacking the 89 N-terminal residues, LjSK1_K167A, LjSK1_Y298A, and native LjSK1 at 21 days post inoculation with rhizobium. Control roots were transformed with the empty T-DNA vector. Values shown are the average ± SEM of n = 6–16 individual hairy roots per construct. Letters above each graph indicate statistically significant differences (p <0.05) between samples using One-way ANOVA followed by Fischer's LSD post-hoc comparison.

Fig. 7 in Mutagenesis of a Lotus japonicus GSK3β/Shaggy-like kinase reveals functionally conserved regulatory residues

Fig. 7. Appearance of whole plants and nodules of L. japonicus hairy root lines transformed with the different LjSK1 variants. A, F) Control (empty vector); B, G) native LjSK1; C, H) LjSK1 K167A; D, I) LjSK1 Y298A; E, J) LjSK190-467. A-E) Representative whole plants with regenerated hairy roots. F-J) Images of nodules on regenerated hairy roots taken in bright-field (top panels) and with an RFP filter to visualize rhizobium colonisation (bottom panels). Scale bars in A-E are 5 cm and in F-G 2 mm.

Fig. 6. Western blot analysis with a p in Mutagenesis of a Lotus japonicus GSK3β/Shaggy-like kinase reveals functionally conserved regulatory residues

Fig. 6. Western blot analysis with a p-GSK-3α/β (6D3) (Santa Cruz Biotechnology, Inc.) monoclonal antibody raised against a phosphopeptide corresponding to amino acids residues surrounding Tyr279 of human GSK3α and Tyr216 of human GSK3β. Lane 1: recombinant LjSK1 and lane 2: LjSK1 Y298A variant. Both proteins have a GST-tag.

Fig. 4 in Mutagenesis of a Lotus japonicus GSK3β/Shaggy-like kinase reveals functionally conserved regulatory residues

Fig. 4. pH (A) and temperature (B) curves for LjSK1 together with standard error bars. Points represent the average value of three measurements. RLU refers to Relative Light Units and ΔRLU is for the difference between a control sample (without enzyme) and the corresponding sample with enzyme. Measurements were performed as described in section 5.3.

Fig. 2. A in Mutagenesis of a Lotus japonicus GSK3β/Shaggy-like kinase reveals functionally conserved regulatory residues

Fig. 2. A homology model of the LjSK1 – ATP complex based on the structure of human GSK3β (PDB:1J1B) (Aoki et al., 2004) after refinement with molecular dynamics simulations and docking of the ATP molecule at the ATP binding site. N- and C-terminal lobes are indicated by different colors and the G-loop and the activation loop are indicated in purple and green, respectively. Mutated residues are shown as stick models. Figure created using Pymol (DeLano, 2002). (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Fig. 1 in Mutagenesis of a Lotus japonicus GSK3β/Shaggy-like kinase reveals functionally conserved regulatory residues

Fig. 1. Alignment of the primary structure of LjSK1, human GSK3β and AtSK3-2. Identical residues are shown in bold. Residues mutated to alanine are boxed. Residues constituting G-loop and the activation loop are shown in grey boxes and the respective structural feature is indicated. Black arrows indicate residues predicted to be in close proximity to the phosphates of ATP. Gaps, represented by dashes, were introduced into the sequences to optimize the alignment.

Ensartinib as Adjuvant Treatment in Anaplastic Lymphoma Kinase (ALK) Positive Non-small Cell Lung Cancer

ClinicalTrials.gov study NCT05341583. IPD Sharing: NO. Countries: 1. Publications: 0.

Rapamycin Treatment for Activated Phosphoinositide 3-Kinase δ Syndrome

ClinicalTrials.gov study NCT03383380. IPD Sharing: NO. Countries: 1. Publications: 6.

controlledIPD-YESFeb 2026View details →

Erlotinib in Combination With Select Tyrosine Kinase Inhibitors in Adult Patients With Advanced Solid Tumors

ClinicalTrials.gov study NCT06161558. IPD Sharing: YES. Countries: 1. Publications: 3.

Sorafenib Treatment in Non-Small Cell Lung Cancer After Failure of Epidermal Growth Factor Receptor-tyrosine Kinase Inhibitor

ClinicalTrials.gov study NCT00922584. IPD Sharing: Not stated. Countries: 1. Publications: 1.

controlledIPD-YESFeb 2026View details →

Lurbinectedin With Berzosertib, an ATR Kinase Inhibitor in Small Cell Cancers and High-Grade Neuroendocrine Cancers

ClinicalTrials.gov study NCT04802174. IPD Sharing: YES. Countries: 1. Publications: 1.

Phase Ib Study of PI3(Phosphoinositol 3)-Kinase Inhibitor Copanlisib With MEK (Mitogen-activated Protein Kinase) Inhibitor Refametinib (BAY86-9766) in Patients With Advanced Cancer

ClinicalTrials.gov study NCT01392521. IPD Sharing: Not stated. Countries: 3. Publications: 1.

Phosphatidylinositol 3-kinase (PI3K) Alpha iNhibition In Advanced Breast Cancer

ClinicalTrials.gov study NCT02506556. IPD Sharing: Not stated. Countries: 1. Publications: 3.

DNAJB1-PRKACA Fusion Kinase Peptide Vaccine Combined With Nivolumab and Ipilimumab for Patients With Fibrolamellar Hepatocellular Carcinoma

ClinicalTrials.gov study NCT04248569. IPD Sharing: NO. Countries: 1. Publications: 3.

A Study for Tyrosine Kinase Inhibitors Discontinuation

ClinicalTrials.gov study NCT02897245. IPD Sharing: NO. Countries: 1. Publications: 1.

A Study of ASP8273 in Epidermal Growth Factor Receptor (EGFR) Tyrosine Kinase Inhibitor-Naïve Patients With Non-Small Cell Lung Cancer Harboring EGFR Mutations

ClinicalTrials.gov study NCT02500927. IPD Sharing: NO. Countries: 1. Publications: 1.

A Study in Rheumatoid Arthritis With an Investigational Oral p38 MAP Kinase Inhibitor VX-702

ClinicalTrials.gov study NCT00395577. IPD Sharing: Not stated. Countries: 6. Publications: 1.

Low-dose Chemotherapy Combine With Tyrosine Kinase Inhibitor to Treat ph+ Acute Lymphoblastic Leukemia Patients

ClinicalTrials.gov study NCT02690922. IPD Sharing: NO. Countries: 1. Publications: 2.