Results 71 to 80 of about 2,028,352 (356)

Red blood cell membrane disorders [PDF]

British Journal of Haematology, 1999
The recent discovery of the specific molecular defects in many patients with hereditary spherocytosis and hereditary elliptocytosis/pyropoikilocytosis partially clarifies the molecular pathology of these diseases. HE and HPP are caused by defects in the horizontal interactions that hold the membrane skeleton together, particularly the critical spectrin
W T, Tse, S E, Lux
openaire   +2 more sources

YAP1::TFE3 mediates endothelial‐to‐mesenchymal plasticity in epithelioid hemangioendothelioma

Molecular Oncology, EarlyView.
The YAP1::TFE3 fusion protein drives endothelial‐to‐mesenchymal transition (EndMT) plasticity, resulting in the loss of endothelial characteristics and gain of mesenchymal‐like properties, including resistance to anoikis, increased migratory capacity, and loss of contact growth inhibition in endothelial cells.
Ant Murphy, Samuel Hartzler, Paula A. Vargas Carranza, Shyaman Jayasundara, Madison E. Yates, Nimod D. Janson, Bozhi Liu, Annaleigh Benton, Majid Kazemian, Jason A. Hanna   +9 more
wiley   +1 more source

Glycophorin-C sialylation regulates Lu/BCAM adhesive capacity during erythrocyte aging

Blood Advances, 2018
: Lutheran/basal cell adhesion molecule (Lu/BCAM) is a transmembrane adhesion molecule expressed by erythrocytes and endothelial cells that can interact with the extracellular matrix protein laminin-α5.
T.R.L. Klei, D.Z. de Back, P.J. Asif, P.J.J.H. Verkuijlen, M. Veldthuis, P.C. Ligthart, J. Berghuis, E. Clifford, B.M. Beuger, T.K. van den Berg, R. van Zwieten, W. El Nemer, R. van Bruggen   +12 more
doaj   +1 more source

Emerging role of ARHGAP29 in melanoma cell phenotype switching

Molecular Oncology, EarlyView.
This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster, Melanie Kappelmann‐Fenzl, Anja Katrin Bosserhoff, Nicole Rachinger   +3 more
wiley   +1 more source

A fractal approach to the rheology of concentrated cell suspensions

, 2007
Results on the rheological behavior of novel CHO cell suspensions in a large range of concentrations are reported. The concentration dependent yield stress and elastic plateau modulus are formalized in the context of fractal aggregates under shear, and ...
Duperray, Alain, Iordan, Andreea, Verdier, Claude   +2 more
core   +2 more sources

Gut microbiota diversity is prognostic in metastatic hormone receptor‐positive breast cancer patients receiving chemotherapy and immunotherapy

Molecular Oncology, EarlyView.
In this exploratory study, we investigated the relationship between the gut microbiota and outcome in patients with metastatic hormone receptor‐positive breast cancer, treated in a randomized clinical trial with chemotherapy alone or chemotherapy in combination with immune checkpoint blockade.
Andreas Ullern, Kristian Holm, Nikolai Kragøe Andresen, Andreas Hagen Røssevold, Corinna Bang, Bjørn Naume, Johannes R. Hov, Jon Amund Kyte   +7 more
wiley   +1 more source

Numerical-experimental observation of shape bistability of red blood cells flowing in a microchannel [PDF]

, 2017
Red blood cells flowing through capillaries assume a wide variety of different shapes owing to their high deformability. Predicting the realized shapes is a complex field as they are determined by the intricate interplay between the flow conditions and ...
Gekle, Stephan, Guckenberger, Achim, John, Thomas, Kihm, Alexander, Wagner, Christian   +4 more
core   +2 more sources

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

Molecular Oncology, EarlyView.
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu, Jianlei Zhao, Aaban Asfar Azmi, Avanti Gupte, Jenna Thibodeau, Shuang Liu, Jinli Yang, Guan Wang, Holly Edwards, Lisa A. Polin, Juiwanna Kushner, Sijana H. Dzinic, Kathryn White, Julie Boerner, Maik Hüttemann, Jay Yang, Yue Wang, Jeffrey W. Taub, Yubin Ge   +18 more
wiley   +1 more source

Whiteout: a social history of sickle cell disease in Ontario, Canada

Critical Public Health
What does it mean to develop health policies and services for diseases that are socially constructed as racialized in a country that continuously erases race?
Sinthu Srikanthan
doaj   +1 more source

Adaptaquin is selectively toxic to glioma stem cells through disruption of iron and cholesterol metabolism

Molecular Oncology, EarlyView.
Adaptaquin selectively kills glioma stem cells while sparing differentiated brain cells. Transcriptomic and proteomic analyses show Adaptaquin disrupts iron and cholesterol homeostasis, with iron chelation amplifying cytotoxicity via cholesterol depletion, mitochondrial dysfunction, and elevated reactive oxygen species.
Adrien M. Vaquié, Davod R. Shah, Eliane E. S. Brechbühl, Michael McNicholas, Zhaoyang Xu, John H. Stockley, Laura Morcom, Diana Gold Diaz, Gemma C. Girdler, Rachel V. Seear, Gabriel Balmus, Rajiv R. Ratan, Harry Bulstrode, James A. Nathan, Manav Pathania, Kevin M. Brindle, David H. Rowitch   +16 more
wiley   +1 more source