Peter W. Abel
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View article: Triggering Receptor Expressed on Myeloid Cells-1 (TREM-1) in Inflammation and Disease: Mechanisms, Therapeutic Potential, and Future Directions
Triggering Receptor Expressed on Myeloid Cells-1 (TREM-1) in Inflammation and Disease: Mechanisms, Therapeutic Potential, and Future Directions Open
Triggering receptor expressed on myeloid cells-1 (TREM-1), a member of the immunoglobulin superfamily, plays a crucial role in amplifying inflammatory responses, thereby contributing to the pathogenesis and progression of various inflammat…
View article: Supplementary Figure 2 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
Supplementary Figure 2 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4 Open
Supplementary Figure 2 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
View article: Data from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
Data from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4 Open
Aberrant signaling through G-protein coupled receptors promotes metastasis, the major cause of breast cancer death. We identified regulator of G-protein signaling 4 (RGS4) as a novel suppressor of breast cancer migration and invasion, impo…
View article: Supplementary Figure Legends 1-3 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
Supplementary Figure Legends 1-3 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4 Open
Supplementary Figure Legends 1-3 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
View article: Supplementary Figure 1 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
Supplementary Figure 1 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4 Open
Supplementary Figure 1 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
View article: Supplementary Figure 1 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
Supplementary Figure 1 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4 Open
Supplementary Figure 1 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
View article: Supplementary Figure 3 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
Supplementary Figure 3 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4 Open
Supplementary Figure 3 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
View article: Data from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
Data from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4 Open
Aberrant signaling through G-protein coupled receptors promotes metastasis, the major cause of breast cancer death. We identified regulator of G-protein signaling 4 (RGS4) as a novel suppressor of breast cancer migration and invasion, impo…
View article: Supplementary Figure Legends 1-3 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
Supplementary Figure Legends 1-3 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4 Open
Supplementary Figure Legends 1-3 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
View article: Supplementary Figure 3 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
Supplementary Figure 3 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4 Open
Supplementary Figure 3 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
View article: Supplementary Figure 2 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
Supplementary Figure 2 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4 Open
Supplementary Figure 2 from Breast Cancer Migration and Invasion Depend on Proteasome Degradation of Regulator of G-Protein Signaling 4
View article: The Evaluation of Novel Targets for CAR T Therapy in Glioblastoma
The Evaluation of Novel Targets for CAR T Therapy in Glioblastoma Open
AIMS The basis of this research revolves around the issue of limited expression of targetable tumour-specific antigens, heterogeneity, and mutation, which impede the development and success of CAR T therapy for glioblastoma. The research w…
View article: KMT5B is required for early motor development
KMT5B is required for early motor development Open
Disruptive variants in lysine methyl transferase 5B (KMT5B/SUV4-20H1) have been identified as likely-pathogenic among humans with neurodevelopmental phenotypes including motor deficits (i.e., hypotonia and motor delay). However, the role t…
View article: Airway relaxation mechanisms and structural basis of osthole for improving lung function in asthma
Airway relaxation mechanisms and structural basis of osthole for improving lung function in asthma Open
A compound derived from a traditional Chinese medicine targets a phosphodiesterase to induce airway relaxation.
View article: Progressive cardiorespiratory dysfunction in Kv1.1 knockout mice may provide temporal biomarkers of pending sudden unexpected death in epilepsy (SUDEP): The contribution of orexin
Progressive cardiorespiratory dysfunction in Kv1.1 knockout mice may provide temporal biomarkers of pending sudden unexpected death in epilepsy (SUDEP): The contribution of orexin Open
Objective Immediately preceding sudden unexpected death in epilepsy (SUDEP), patients experienced a final generalized tonic‐clonic seizure (GTCS), rapid ventilation, apnea, bradycardia, terminal apnea, and asystole. Whether a progressive p…
View article: CAR-T: expanding the horizons
CAR-T: expanding the horizons Open
Immunotherapy in cancer treatment The human immune system provides a powerful response to invading organisms, destroying bacteria and viruses, as well as aberrant cells that turn cancerous and proliferate uncontrollably. The enquiring mind…
View article: Up-regulated miR-133a orchestrates epithelial-mesenchymal transition of airway epithelial cells
Up-regulated miR-133a orchestrates epithelial-mesenchymal transition of airway epithelial cells Open
Dysregulation of microRNAs (miRNAs) contributes to epithelial-mesenchymal transition (EMT) of cancer, but the pathological roles of miRNAs in airway EMT of lung diseases remains largely unknown. We performed sequencing and real-time PCR an…
View article: Respiratory dysfunction progresses with age in <i>Kcna1</i>‐null mice, a model of sudden unexpected death in epilepsy
Respiratory dysfunction progresses with age in <i>Kcna1</i>‐null mice, a model of sudden unexpected death in epilepsy Open
Summary Objective Increased breathing rate, apnea, and respiratory failure are associated with sudden unexpected death in epilepsy ( SUDEP ). We recently demonstrated the progressive nature of epilepsy and mortality in Kcna1 −/− mice, a mo…
View article: Targeting Androgen Receptor and TRAIL: A Novel Treatment Paradigm for Breast Cancer
Targeting Androgen Receptor and TRAIL: A Novel Treatment Paradigm for Breast Cancer Open
BACKGROUND & OBJECTIVE: TRAIL (TNF-related apoptosis-inducing ligand) is a promising cancer therapeutic agent due to its minimal toxicity to normal tissues and remarkable apoptotic activity in tumors. However, most breast cancer cells are …
View article: IMST-12. INVESTIGATION INTO MECHANISMS OF IMMUNOSUPPRESSION IN GLIOMA
IMST-12. INVESTIGATION INTO MECHANISMS OF IMMUNOSUPPRESSION IN GLIOMA Open
Glioblastoma induces immunosuppressive effects by several, redundant mechanisms, TGF-β/VEGF signalling pathway, IL-2Rα/CD25-mediated, CTLA-4/PD-1/PD-L1 immune checkpoint interaction and STAT3 activation. All of these mechanisms have been i…
View article: Upregulation of RGS2: a new mechanism for pirfenidone amelioration of pulmonary fibrosis
Upregulation of RGS2: a new mechanism for pirfenidone amelioration of pulmonary fibrosis Open
Endogenous RGS2 exhibits anti-fibrotic functions. Upregulated RGS2 contributes significantly to the anti-fibrotic effects of pirfenidone.