Results 211 to 220 of about 6,880,999 (291)

A Mutation in Damage-Specific DNA Binding Protein One (ddb-1) Underlies the Phenotype of the No-Marginal-Zone (nmz) Mutant Zebrafish

Kailey Jerome, Aria Gish, Taylor Aakre, Taylor Brend, Mélanie Grenier, Christina L. Johnson, Jaxon Gronneberg, Colin O’Neill, Lucas Radermacher, Tristan Darland   +9 more
openalex   +1 more source

Degradation of a Mutant Secretory Protein, α1-Antitrypsin Z, in the Endoplasmic Reticulum Requires Proteasome Activity [PDF]

, 1996
Dongfeng Qu, Jeffrey Teckman, Satoshi Ōmura, David H. Perlmutter   +3 more
openalex   +1 more source

Plecstatin inhibits hepatocellular carcinoma tumorigenesis and invasion through cytolinker plectin

Molecular Oncology, EarlyView.
The ruthenium‐based metallodrug plecstatin exerts its anticancer effect in hepatocellular carcinoma (HCC) primarily through selective targeting of plectin. By disrupting plectin‐mediated cytoskeletal organization, plecstatin inhibits anchorage‐dependent growth, cell polarization, and tumor cell dissemination.
Zuzana Outla, Jan Kosla, Magdalena Prechova, Lukas Frick, Patricia Bortel, Yasmin Borutzki, Andrea Bileck, Christopher Gerner, Samuel M. Meier‐Menches, Selma Osmanagic‐Myers, Martin Gregor   +10 more
wiley   +1 more source

Erratum to "Not so Rare: Diseases based on Mutant Proteins Controlling Endoplasmic Reticulum-Mitochondria Contact (MERC) Tethering". [PDF]

Contact (Thousand Oaks)
europepmc   +1 more source

Environments of the four tryptophans in the extracellular domain of human tissue factor: comparison of results from absorption and fluorescence difference spectra of tryptophan replacement mutants with the crystal structure of the wild-type protein

, 1995
C. A. Hasselbacher, E. V. Rusinova, Eli Waxman, Radda Rusinova, Ronald A. Kohanski, Wan Yee Lam, Anirban Guha, Jiangfeng Du, Tai‐Shun Lin, Igor Polikarpov   +9 more
openalex   +1 more source

Recurrent cancer‐associated ERBB4 mutations are transforming and confer resistance to targeted therapies

Molecular Oncology, EarlyView.
We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala, Sini Ahonen, Sara Peltola, Aura Tuohisto‐Kokko, Olaya Esparta, Peppi Suominen, Anne Jokilammi, Iman Farahani, Deepankar Chakroborty, Nikol Dibus, Steffen Boettcher, Tomi T. Airenne, Mark S. Johnson, Lisa D. Eli, Klaus Elenius, Kari J. Kurppa   +15 more
wiley   +1 more source

Molecular Modelling-Based Investigations of a Mutant Protein in Patients with Hearing Loss

, 2014
Kazunori Namba
openalex   +2 more sources

Interactions of normal and mutant vesicular stomatitis virus matrix proteins with the plasma membrane and nucleocapsids [PDF]

, 1994
L D Chong, J K Rose
openalex   +1 more source

Peroxidasin enables melanoma immune escape by inhibiting natural killer cell cytotoxicity

Molecular Oncology, EarlyView.
Peroxidasin (PXDN) is secreted by melanoma cells and binds the NK cell receptor NKG2D, thereby suppressing NK cell activation and cytotoxicity. PXDN depletion restores NKG2D signaling and enables effective NK cell–mediated melanoma killing. These findings identify PXDN as a previously unrecognized immune evasion factor and a potential target to improve
Hsu‐Min Sung, David Bickel, Lena C. M. Krause, Daria Ezeriņa, Christian Ickes, Julian Wojtachnia, Christine S. Gibhardt, Magdalena Shumanska, Khadija Wahni, Andrea Paluschkiwitz, Julia Malo Pueyo, Ekaterina Baranova, Wim Vranken, Hedwig Stanisz, Ioana Stejerean‐Todoran, Michael P. Schön, Joris Messens, Ivan Bogeski   +17 more
wiley   +1 more source

Phenotypic and genotypic characterization of single circulating tumor cells in the follow‐up of high‐grade serous ovarian cancer

Molecular Oncology, EarlyView.
Single circulating tumor cells (sCTCs) from high‐grade serous ovarian cancer patients were enriched, imaged, and genomically profiled using WGA and NGS at different time points during treatment. sCTCs revealed enrichment of alterations in Chromosomes 2, 7, and 12 as well as persistent or emerging oncogenic CNAs, supporting sCTC identity.
Carolin Salmon, Rui P. L. Neves, Nikolas H. Stoecklein, Sven‐Thorsten Liffers, Jens Siveke, Jan D. Kuhlmann, Pauline Wimberger, Paul Buderath, Rainer Kimmig, Sabine Kasimir‐Bauer   +9 more
wiley   +1 more source