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Kindlin-2 regulates colonic cancer stem-like cells survival and self-renewal via Wnt/β-catenin mediated pathway.
Cell Signal
January 2024
Department of Microbiology, Gastrointestinal Disease Lab, Room 522 Academic Building, Central University of Punjab, School of Basic Science, VPO Ghudda, Bathinda, Punjab 151401, India. Electronic address:
Background: Cancer Stem Cells (CSCs) have emerged as a critical mediator in recurrence and resistance in cancers. Kindlin-isoform (1 and 2) binds with cytoplasmic β-tail of integrin and are essential co-activators of integrin function. Given their important function in regulating cancer hallmarks such as cell proliferation, invasion, migration, and metastasis, we hypothesize that it might play a critical role in CSC growth, survival, and self-renewal of colon cancer.
View Article and Find Full Text PDFKindlin-2 in myoepithelium controls luminal progenitor commitment to alveoli in mouse mammary gland.
Cell Death Dis
October 2023
Program for Cancer and Cell Biology, Department of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences; Peking University International Cancer Institute; MOE Key Laboratory of Carcinogenesis and Translational Research and State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, 100191, Beijing, China.
Myoepithelium plays an important role in mammary gland development, but less is known about the molecular mechanism underlying how myoepithelium controls acinus differentiation during gestation. Herein, we found that loss of Kindlin-2 in myoepithelial cells impaired mammary morphogenesis, alveologenesis, and lactation. Using five genetically modified mouse lines combined with single-cell RNA sequencing, we found a Kindlin-2-Stat3-Dll1 signaling cascade in myoepithelial cells that inactivates Notch signaling in luminal cells and consequently drives luminal progenitor commitment to alveolar cells identity.
View Article and Find Full Text PDFKindlin stabilizes the talin·integrin bond under mechanical load by generating an ideal bond.
Proc Natl Acad Sci U S A
June 2023
Department of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried 82152, Germany.
Integrin-mediated adhesion is essential for metazoan life. Integrin binding to ligand requires an activation step prior to binding ligand that depends on direct binding of talin and kindlin to the β-integrin cytoplasmic tail and the transmission of force from the actomyosin via talin to the integrin-ligand bonds. However, the affinity of talin for integrin tails is low.
View Article and Find Full Text PDFKindlin-2 Promotes Chondrogenesis and Ameliorates IL-1beta-Induced Inflammation in Chondrocytes Cocultured with BMSCs in the Direct Contact Coculture System.
Oxid Med Cell Longev
April 2022
Department of Orthopedics, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
The osteoarthritis caused by trauma or inflammation is associated with severe patient morbidity and economic burden. Accumulating studies are focusing on the repair of articular cartilage defects by constructing tissue-engineered cartilage. Recent evidence suggests that optimizing the source and quality of seed cells is one of the key points of cartilage tissue engineering.
View Article and Find Full Text PDFKindlin-3 in Immune Cells Is Required to Suppress Prostate Cancer Tumor Growth in Mice.
Anticancer Res
March 2022
Versiti Blood Research Institute, Milwaukee, WI, U.S.A.;
Background/aim: Kindlins are essential integrin activators. Kindlin-1 and kindlin-2 are often concomitantly expressed in epithelial tumor cells and participate in regulating tumor malignancy. However, it remains unclear whether kindlin-3, the one expressed in immune cells, also plays a role in regulating tumor malignancy.
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