Zobrazeno 1 - 10
of 20
pro vyhledávání: '"Kyle M. Draheim"'
Autor:
Jiwon Yang, Jing Jiao, Kyle M. Draheim, Guoxiang Yang, Hongyuan Yang, Li‐Chin Yao, Leonard D. Shultz, Dale L. Greiner, Deepa Rajagopal, Sandrine Vessillier, Curtis C. Maier, Sunish Mohanan, Danying Cai, Mingshan Cheng, Michael A. Brehm, James G. Keck
Publikováno v:
The FASEB Journal. 37
Publikováno v:
Journal of Biological Chemistry. 292:1884-1898
Binding of ICAP1 (integrin cytoplasmic domain-associated protein-1) to the cytoplasmic tails of β1 integrins inhibits integrin activation. ICAP1 also binds to KRIT1 (Krev interaction trapped-1), a protein whose loss of function leads to cerebral cav
Publikováno v:
J Biol Chem
Nuclear accumulation of the small phosphoprotein integrin cytoplasmic domain–associated protein-1 (ICAP1) results in recruitment of its binding partner, Krev/Rap1 interaction trapped-1 (KRIT1), to the nucleus. KRIT1 loss is the most common cause of
Publikováno v:
Cancer Research. 80:1672-1672
Preclinical oncology studies frequently use patient-derived xenograft (PDX) tumor models and the efficacy of the test therapy is evaluated by measuring changes in tumor volume. Subcutaneous (SQ) implantation of tumors is most widely used in oncology
Publikováno v:
The Journal of Immunology. 204:91.31-91.31
Although immuno-oncology therapies such as checkpoint inhibitors, bispecific antibodies and CAR-T cells have been successfully used as cancer treatments, they can have severe adverse effects such as cytokine release syndrome (CRS). The animal models
Autor:
Titus J. Boggon, Giulia Villari, Rong Zhang, Oriana S. Fisher, David A. Calderwood, Xiaofeng Li, Kyle M. Draheim
Publikováno v:
The Journal of Cell Biology
CCM2–CCM3 interactions protect CCM2 and CCM3 from proteasomal degradation, and both CCM2 and CCM3 are required for normal endothelial cell network formation.
Mutations in the essential adaptor proteins CCM2 or CCM3 lead to cerebral cavernous m
Mutations in the essential adaptor proteins CCM2 or CCM3 lead to cerebral cavernous m
Publikováno v:
Oncogene
Large-scale genetic analyses of human tumor samples have been used to identify novel oncogenes, tumor suppressors and prognostic factors, but the functions and molecular interactions of many individual genes have not been determined. In this study we
Autor:
Veena Krishnamoorthy, Kathleen Cullion, Nicole Hermance, George N. Nikov, Kyle M. Draheim, Christopher Ware, Michelle A. Kelliher, Jennifer Tammam, Pradip K. Majumder, Vishva Mitra Sharma
Publikováno v:
Blood. 113:6172-6181
Mutations in NOTCH1 are frequently detected in patients with T-cell acute lymphoblastic leukemia (T-ALL) and in mouse T-ALL models. Treatment of mouse or human T-ALL cell lines in vitro with γ-secretase inhibitors (GSIs) results in growth arrest and
Publikováno v:
Cell Cycle. 6:927-930
The Notch receptor family and its ligands (Delta-like and Jagged) have been found deregulated in several human cancers. We and the Aster/Pear group recently identified c-myc as a direct transcriptional target gene of the Notch1 pathway in T cell acut
Autor:
Veena Krishnamoorthy, Jennifer A. Calvo, Leslie A. Cunningham, Manoj Bhasin, Anthony J. Capobianco, Vishva Mitra Sharma, Levi J. Beverly, Nicole Hermance, Michelle A. Kelliher, Kyle M. Draheim
Publikováno v:
Molecular and Cellular Biology. 26:8022-8031
Recent work with mouse models and human leukemic samples has shown that gain-of-function mutation(s) in Notch1 is a common genetic event in T-cell acute lymphoblastic leukemia (T-ALL). The Notch1 receptor signals through a gamma-secretase-dependent p