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891 results for “Apoptosis”

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geo24/100

Human platelet lysate enhances in vivo activity of CAR-Vδ2 T cells by reducing cellular senescence and apoptosis

GEO Series GSE247760. Homo sapiens. 8 samples. Type: Expression profiling by high throughput sequencing.

openGEO-OpenAug 2024View details →
geo24/100

TTF-1-regulated miR-532-5p targets KRAS and MKL2 oncogenes and induces apoptosis in lung adenocarcinoma [rt-pcr]

GEO Series GSE83838. Homo sapiens. 4 samples. Type: Expression profiling by RT-PCR.

openGEO-OpenJun 2017View details →
geo24/100

Mettl14-dependent m6A modification controls iNKT cells development and function by regulating p53-dependent apoptosis pathway and TCR signaling

GEO Series GSE189339. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.

openGEO-OpenMar 2022View details →
geo24/100

Vitamin C Promotes Apoptosis in Breast Cancer Cells by Increasing TRAIL Expression

GEO Series GSE121093. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.

openGEO-OpenOct 2018View details →
geo24/100

XPO1 blockade with KPT-330 promotes apoptosis in Cutaneous T- cell Lymphoma by activating the p53-p21 and p27 pathways

GEO Series GSE262491. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.

openGEO-OpenApr 2024View details →
geo24/100

Turkey B-cell Transcriptome Profile During Turkey Hemorrhagic Enteritis Virus (THEV) Infection Highlights Upregulated Apoptosis and Breakdown Pathways That May Mediate Immunosuppression

GEO Series GSE286211. Meleagris gallopavo. 19 samples. Type: Expression profiling by high throughput sequencing.

openGEO-OpenApr 2025View details →
geo24/100

p53-induced apoptosis is specified by a translation program regulated by PCBP2 and DHX30.

GEO Series GSE95024. Homo sapiens. 24 samples. Type: Expression profiling by high throughput sequencing.

openGEO-OpenMar 2020View details →
zenodo24/100

MicroRNA-221 promotes cell proliferation and inhibit apoptosis in osteosarcoma cells via directly targeting FBXW11 and regulating the Wnt signaling

<p><strong>Figure 1.</strong> miR-221 expression is significantly high in human clinical tissues and cell lines of OS. The expression levels of miR-221 in 30 pairs of OS tissues and their adjacent, non-cancerous normal bone tissues (Normal) (A) and the human osteoblastic cell line hFOB 1.19 and OS cell lines (B) are detected by qRT-PCR. U6 is used as the internal control. **<em>P</em> &lt; 0.01 and ***<em>P</em> &lt; 0.001.</p> <p><strong>Figure 2. </strong>Attenuating miR-221 expression inhibits OS cell proliferation and increase apoptosis. MiR-221 inhibitor is transfected into MG-63-A16 (A) or U2OS cells (B) and induces an obviously lower proliferation rate compared with that in control groups. Further, miR-221 inhibitor is transfected into MG-63-A16 (C) and U2OS cells (D) and triggers a significantly higher apoptosis than controls. And that, the significantly down-regulated Ki67 expression in MG-63-A16 (E) and U2OS cells (F) were observed compared with that in the controls. **<em>P</em> &lt; 0.01 and ***<em>P</em> &lt; 0.001.</p> <p><strong>Figure 3. </strong>FBXW11 can directly target to miR-221. (A) An potential target of miR-221, called as FBXW11 has been predicted by bioinformatics-based target prediction analysis, and the binding site is on the 3&rsquo;UTR of FBXW11. (B) RT-PCR analysis of FBXW11 expression in the OS tumor tissues and noncancerous counterparts. (C) The obviously down-regulated expression levels of FBXW11 mRNA are observed in OS cell lines compared with those in hFOB 1.19 cells. (D) A negative Spearman&rsquo;s correlation between miR-221 and FBXW11 mRNA levels was observed in 30 OS tumor tissues. (E) The significantly decreased luciferase activity driven by 3&rsquo;UTR of FBXW11 is observed in the miR-211 mimic group and the 3&rsquo;UTR-MUT group and negative control are as control. (F) The down-regulation of miR-221 induces a dramatic overexpression of FBXW11 protein. (G) A distinctly lower cell proliferation rate is observed in the group of pcDNA-FBXW11 compared with control. (H) An obviously higher apoptosis is observed in the group of pcDNA-FBXW11 than control. (I) The significantly decreased Ki67 expression is detected in the pcDNA-FBXW11 group than control. **<em>P</em> &lt; 0.01 and ***<em>P</em> &lt; 0.001.</p> <p><strong>Figure 4.</strong> miR-221 and FBXW11 regulate cell proliferation and apoptosis in OS through inhibiting Wnt signaling. (A) The markedly down-regulated expression levels of &beta;-catenin, cyclin D1 and c-myc were detected in the group of miR-221 inhibitor compared with controls. (B) The obviously decreased expression levels of &beta;-catenin, cyclin D1 and c-myc were determined in the pcDNA-FBXW11 group compared with controls. **<em>P</em> &lt; 0.01 and ***<em>P</em> &lt; 0.001.</p> <p><strong>Figure 5. </strong>The effect of Wnt signaling on the cell proliferation and apoptosis of OS cell lines. A distinctly lower cell proliferation rate (A and B) and an obviously higher apoptosis rate (C and D) were detected in the Wnt1 siRNA groups (siRNA1, siRNA2) than si-control, and similar results were observed in the CGP049090 group. (E and F) The obviously decreased Ki67 expression were detected in the Wnt1 siRNA groups compared with si-control, and similar results were observed in the CGP049090 group. **<em>P</em> &lt; 0.01 and ***<em>P</em> &lt; 0.001.</p>

opencc-by-4.0Apr 2020View details →
dryad24/100

Data from: Enhancement of apoptosis by titanium alloy internal fixations during microwave treatments for fractures: an animal study

Objective: Microwaves are used in one method of physical therapy and can increase muscle tissue temperature which is useful for improving muscle, tendon and bone injuries. In the study, we sought to determine whether titanium alloy internal fixations influence apoptosis in tissues subjected to microwave treatments at 2,450 MHz and 40 W during the healing of fractures because this issue is not yet fully understood. Methods: In this study, titanium alloy internal fixations were used to treat 3.0-mm transverse osteotomies in the middle of New Zealand rabbits' femurs. After the operation, 30-day microwave treatments were applied to the 3.0 mm transverse osteotomies 3 days after the operation. The changes in the temperatures of the muscle tissues in front of the implants or the 3.0 mm transverse osteotomies were measured during the microwave treatments. To characterize the effects of titanium alloy internal fixations on apoptosis in the muscles after microwave treatment, we performed TUNEL assays, fluorescent real-time (quantitative) PCR, western blotting analyses, reactive oxygen species (ROS) detection and transmission electron microscopy examinations. Results: The temperatures were markedly increased in the animals with the titanium alloy implants. Apoptosis in the muscle cells of the implanted group was significantly more extensive than that in the non-implanted control group at different time points. Transmission electron microscopy examinations of the skeletal muscles of the implanted groups revealed muscular mitochondrial swelling, vacuolization. ROS, Bax and Hsp70 were up-regulated, and Bcl-2 was down-regulated in the implanted group. Conclusion: Our results suggest that titanium alloy internal fixations caused greater muscular tissue cell apoptosis following 2,450 MHz, 40 W microwave treatments in this rabbit femur fracture models.

opencc-zeroDec 2014View details →
dryad24/100

Data from: Surprising complexity of the ancestral apoptosis network

Apoptosis, one of the main types of programmed cell death, is regulated and performed by a complex protein network. Studies in model organisms, mostly in the nematode C. elegans, identified a relatively simple apoptotic network consisting of only a few proteins. However, analysis of several recently sequenced invertebrate genomes, ranging from the cnidarian sea anemone Nematostella vectensis, representing one of the morphologically simplest metazoans, to the deuterostomes sea urchin and amphioxus, contradicts the current paradigm of a simple ancestral network that expanded in vertebrates. Results Here we show that the apoptosome-forming CED-4/Apaf-1 protein, present in single copy in vertebrate, nematode, and insect genomes, had multiple paralogs in the cnidarian-bilaterian ancestor. Different members of this ancestral Apaf-1 family lead to the extant proteins in nematodes/insects and in deuterostomes, explaining significant functional differences between proteins that until now were believed to be orthologous. Similarly, the evolution of the Bcl-2 and caspase protein families appears surprisingly complex and apparently included significant gene loss in nematodes and insects and expansions in deuterostomes. Conclusion The emerging picture of the evolution of the apoptosis network is one of a succession of lineage-specific expansions and losses, which combined with the limited number of "apoptotic" protein families, resulted in apparent similarities between networks in different organisms that mask an underlying complex evolutionary history. Similar results are beginning to surface for other regulatory networks, contradicting the intuitive notion that regulatory networks evolved in a linear way, from simple to complex.

opencc-zeroDec 2006View details →
zenodo24/100

Figure 1 from: Abbas AH, Mahmood AAR, Tahtamouni LH, Al-Mazaydeh ZA, Rammaha MS, Alsoubani F, Al-bayati RI (2021) A novel derivative of picolinic acid induces endoplasmic reticulum stress-mediated apoptosis in human non-small cell lung cancer cells: synthesis, docking study, and anticancer activity. Pharmacia 68(3): 679-692. https://doi.org/10.3897/pharmacia.68.e70654

Figure 1 Synthesis of the target compounds (4–7).

opencc-by-4.0Sep 2021View details →
ClinicalTrials.gov24/100

The Differences of Oocyte Maturation, Granulosa Cell Apoptosis Index Between Electroacupuncture And Sham Groups IVF

ClinicalTrials.gov study NCT03627533. IPD Sharing: NO. Countries: 1. Publications: 0.

closedIPD-NOFeb 2026View details →
ClinicalTrials.gov24/100

Prognostic Role of Inhibitor of Apoptosis Protein Overexpression on Recurrence Rate in Cervical Cancer

ClinicalTrials.gov study NCT06147960. IPD Sharing: Not stated. Countries: 0. Publications: 0.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov24/100

Study of PRoliferation and Apoptosis in Rectal Cancer, Predictive & Prognostic biOmarkers: Histopathology and Imaging

ClinicalTrials.gov study NCT02486094. IPD Sharing: Not stated. Countries: 1. Publications: 0.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov24/100

Brain Death: Inflammatory Response, Apoptosis, and Endotoxin Tolerance

ClinicalTrials.gov study NCT00615225. IPD Sharing: Not stated. Countries: 2. Publications: 0.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov24/100

Ultrasound Biomicroscopy - Apoptosis

ClinicalTrials.gov study NCT00188370. IPD Sharing: Not stated. Countries: 1. Publications: 0.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov24/100

The Role of Apoptosis Associated Markers in Pathogenesis of Pulmonary Tuberculosis

ClinicalTrials.gov study NCT01676155. IPD Sharing: Not stated. Countries: 1. Publications: 0.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov24/100

Evaluation the of Role of Vitamin D Supplement on Tumor Response, Inflammation and Apoptosis in Patients With Stage II or III Colorectal Cancer Receiving Chemotherapy.

ClinicalTrials.gov study NCT07241247. IPD Sharing: Not stated. Countries: 1. Publications: 0.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov24/100

Imaging Apoptosis for Lymphoma Treatment Response

ClinicalTrials.gov study NCT05048732. IPD Sharing: NO. Countries: 1. Publications: 0.

closedIPD-NOFeb 2026View details →
ClinicalTrials.gov24/100

The Effect of Anesthetics on Oxidative Stress and Apoptosis Status in Children

ClinicalTrials.gov study NCT02711280. IPD Sharing: Not stated. Countries: 1. Publications: 0.

restrictedIPD-UNDECIDEDFeb 2026View details →

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International Brain Laboratory public data

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