Thibaut Quillard
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View article: Identification of miR136, miR155, and miR183 in Vascular Calcification in Human Peripheral Arteries
Identification of miR136, miR155, and miR183 in Vascular Calcification in Human Peripheral Arteries Open
Vascular calcification (V) is an independent risk factor for all-cause and cardiovascular mortality. Vascular smooth muscle cells (VSMCs) play a major role in VC as they can acquire mineralizing properties when exposed to osteogenic condit…
View article: ANGPTL6 variant induces cerebral vascular dysfunction and predisposes to intracranial aneurysm in mice
ANGPTL6 variant induces cerebral vascular dysfunction and predisposes to intracranial aneurysm in mice Open
Background Intracranial aneurysm (IA) is a common cerebrovascular abnormality characterized by localized dilation and wall thinning in intracranial arteries, that frequently leads to fatal sub-arachnoid hemorrhage. Pathophysiological mecha…
View article: Identification of miR136, miR155, and miR183 in vascular calcification in human peripheral arteries
Identification of miR136, miR155, and miR183 in vascular calcification in human peripheral arteries Open
Objective Vascular calcification (VC) is an independent risk factor for all-cause and cardiovascular mortality. This process contributes to atherosclerotic plaque disruption and thrombosis when close to the lumen, arterial stiffness, and l…
View article: supplemental figure legend from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression
supplemental figure legend from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression Open
supplemental figure legend
View article: Supplemental Figure 3 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression
Supplemental Figure 3 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression Open
Supp. Figure 3. Tumors were collected after 42 days and HSP70, MET; FAK and MMP9 were evaluated by immunohistochemical analysis. Specimens were scored and estimated in percentage of positive cells.
View article: supplemental figure legend from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression
supplemental figure legend from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression Open
supplemental figure legend
View article: Supplemental Figure 3 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression
Supplemental Figure 3 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression Open
Supp. Figure 3. Tumors were collected after 42 days and HSP70, MET; FAK and MMP9 were evaluated by immunohistochemical analysis. Specimens were scored and estimated in percentage of positive cells.
View article: Supplemental Figure 2 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression
Supplemental Figure 2 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression Open
Supp. Figure 2. HSP90 inhibition induces client proteins degradation.
View article: Supplemental Figure 2 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression
Supplemental Figure 2 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression Open
Supp. Figure 2. HSP90 inhibition induces client proteins degradation.
View article: Supplementary Table S1 and S2 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression
Supplementary Table S1 and S2 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression Open
Primer and antibodies table
View article: Supplementary Table S1 and S2 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression
Supplementary Table S1 and S2 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression Open
Primer and antibodies table
View article: Data from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression
Data from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression Open
Purpose: Despite recent improvements in therapeutic management of osteosarcoma, ongoing challenges in improving the response to chemotherapy warrants the development of new strategies to improve overall patient survival. Among them,…
View article: Supplemental Figure 1 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression
Supplemental Figure 1 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression Open
Supp. Figure 1. HSP90 messenger RNA level is overexpressd in osteosarcoma patients.
View article: Data from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression
Data from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression Open
Purpose: Despite recent improvements in therapeutic management of osteosarcoma, ongoing challenges in improving the response to chemotherapy warrants the development of new strategies to improve overall patient survival. Among them,…
View article: Supplemental Figure 1 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression
Supplemental Figure 1 from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression Open
Supp. Figure 1. HSP90 messenger RNA level is overexpressd in osteosarcoma patients.
View article: Supplementary Figure S6 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Supplementary Figure S6 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
miR-527 and miR-665 regulate metastasis dissemination in vivo.
View article: Supplementary Figure S2 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Supplementary Figure S2 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
miR-527 and miR-665 repress Smad4 and TβRII, respectively.
View article: Data from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Data from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
Primary cancer cell dissemination is a key event during the metastatic cascade, but context-specific determinants of this process remain largely undefined. Multiple reports have suggested that the p53 (TP53) family member p63 (TP63) plays …
View article: Supplementary Figure S1 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Supplementary Figure S1 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
p63-regulated microRNAs target the TGFβ pathway.
View article: Supplementary Figure S5 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Supplementary Figure S5 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
p63 induces TGFβ-mediated metastasis in vivo.
View article: Supplementary Figure S4 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Supplementary Figure S4 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
The p63 and p73-controlled miR network regulates TGFβ induced migration.
View article: Data from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Data from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
Primary cancer cell dissemination is a key event during the metastatic cascade, but context-specific determinants of this process remain largely undefined. Multiple reports have suggested that the p53 (TP53) family member p63 (TP63) plays …
View article: Supplementary Figure S3 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Supplementary Figure S3 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
p63 and p73 regulate SMAD4 and TβRII.
View article: Supplementary Figure S1 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Supplementary Figure S1 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
p63-regulated microRNAs target the TGFβ pathway.
View article: Supplementary Figure Legends from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Supplementary Figure Legends from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
Legend for Supplementary Figures S1-S6
View article: Supplementary Figure S3 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Supplementary Figure S3 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
p63 and p73 regulate SMAD4 and TβRII.
View article: Supplementary Figure S2 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Supplementary Figure S2 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
miR-527 and miR-665 repress Smad4 and TβRII, respectively.
View article: Supplementary Figure S4 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Supplementary Figure S4 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
The p63 and p73-controlled miR network regulates TGFβ induced migration.
View article: Supplementary Figure S5 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Supplementary Figure S5 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
p63 induces TGFβ-mediated metastasis in vivo.
View article: Supplementary Figure S6 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis
Supplementary Figure S6 from ΔNp63α Silences a miRNA Program to Aberrantly Initiate a Wound-Healing Program That Promotes TGFβ-Induced Metastasis Open
miR-527 and miR-665 regulate metastasis dissemination in vivo.