Results 91 to 100 of about 1,667,987 (261)

Generation of TK2 conditional knockout mice.

open access: yes, 2022
Homologous recombination strategy of TK2 conditional knockout mice (A). breeding strategy of producing TK2 heart and skeletal muscle knockout mice (B).
Sophie Curbo (386586)   +4 more
core   +1 more source

Microglial P2Y12 receptor regulates ventral hippocampal CA1 neuronal excitability and innate fear in mice

open access: yesMolecular Brain, 2019
The P2Y12 receptor (P2Y12R) is a purinoceptor that is selectively expressed in microglia in the central nervous system. As a signature receptor, microglial P2Y12R mediates process chemotaxis towards ADP/ATP gradients and is engaged in several ...
Jiyun Peng   +6 more
doaj   +1 more source

Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr‐mutated lung cancer

open access: yesMolecular Oncology, EarlyView.
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura   +19 more
wiley   +1 more source

Maid gene dysfunction promotes hyperobesity via the reduction of adipose tissue inflammation in Mc4r gene-deficient mice

open access: yesScientific Reports
The onset and progression mechanisms of metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) are being studied.
Kyutaro Koyama   +10 more
doaj   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

Thymosin Beta-4 Induces Mouse Hair Growth.

open access: yesPLoS ONE, 2015
Thymosin beta-4 (Tβ4) is known to induce hair growth and hair follicle (HF) development; however, its mechanism of action is unknown. We generated mice that overexpressed Tβ4 in the epidermis, as well as Tβ4 global knockout mice, to study the role of Tβ4
Xiaoyu Gao   +6 more
doaj   +1 more source

Flow Enabled Target Capture Halbach‐based magnetic enrichment increases circulating tumor cell capture from blood in metastatic cancer patients

open access: yesMolecular Oncology, EarlyView.
Pair‐wise comparison of the CellSearch and FETCH enrichment technologies for circulating tumor cells (CTCs) from metastatic breast, prostate, and small cell lung cancer patients shows an increased capture of CTCs using FETCH enrichment. The clinical implementation of circulating tumor cells (CTCs) as a predictive tool for therapy efficacy in the ...
Michiel Stevens   +6 more
wiley   +1 more source

CAF1-knockout mice are more susceptive to lipopolysaccharide-induced acute lung injury

open access: yes, 2016
Jia-Xin Shi,1 Jia-Shu Li,1 Rong Hu,1 Xiao-Min Li,2 Hong Wang3 1Department of Respiratory Medicine, Lianyungang First People’s Hospital, Affiliated Hospital of Xuzhou Medical University, Affiliated Hospital of the Clinical Medical School of Nanjing ...
Li JS, Shi JX, Li XM, Wang H, Hu R
core  

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

open access: yesMolecular Oncology, EarlyView.
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober   +16 more
wiley   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

open access: yesMolecular Oncology, EarlyView.
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder   +10 more
wiley   +1 more source

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