S
Scott R. McKercher
Researcher at Sanford-Burnham Institute for Medical Research
Publications - 42
Citations - 6685
Scott R. McKercher is an academic researcher from Sanford-Burnham Institute for Medical Research. The author has contributed to research in topics: Neural stem cell & Haematopoiesis. The author has an hindex of 26, co-authored 40 publications receiving 6336 citations. Previous affiliations of Scott R. McKercher include University College London & National Foundation for Cancer Research.
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Journal ArticleDOI
Turning Blood into Brain: Cells Bearing Neuronal Antigens Generated in Vivo from Bone Marrow
TL;DR: It is shown that, in a strain of mice incapable of developing cells of the myeloid and lymphoid lineages, transplanted adult bone marrow cells migrated into the brain and differentiated into cells that expressed neuron-specific antigens.
Journal ArticleDOI
Targeted disruption of the PU.1 gene results in multiple hematopoietic abnormalities.
Scott R. McKercher,Bruce E. Torbett,Karen L. Anderson,Gregory W. Henkel,Deborah J. Vestal,Helene Baribault,Michael J. Klemsz,Ann J. Feeney,Gillian E. Wu,Christopher J. Paige,Richard A. Maki +10 more
TL;DR: While the PU.1 protein appears not to be essential for myeloid and lymphoid lineage commitment, it is absolutely required for the normal differentiation of B cells and macrophages.
Journal ArticleDOI
Osteopetrosis in mice lacking haematopoietic transcription factor PU.1
M M Tondravi,Scott R. McKercher,Karen L. Anderson,Jeanne M. Erdmann,M. Quiroz,Robert G. Maki,Steven L. Teitelbaum +6 more
TL;DR: The absence of both osteoclasts and macrophages in PU.1-mutant animals suggests that the transcription factor regulates the initial stages of myeloid differentiation, and that its absence represents the earliest developmental osteopetrotic mutant yet described.
Journal ArticleDOI
Wound Healing in the PU.1 Null Mouse—Tissue Repair Is Not Dependent on Inflammatory Cells
Paul Martin,Deana D'Souza,Julie Martin,Richard Grose,Lisa Cooper,Rich Maki,Scott R. McKercher +6 more
TL;DR: Wound healing studies are reported in the PU.1 null mouse, which is genetically incapable of raising the standard inflammatory response because it lacks macrophages and functioning neutrophils, and it is shown that these "macrophageless" mice are able to repair skin wounds with similar time course to wild-type siblings.
Journal ArticleDOI
Aβ induces astrocytic glutamate release, extrasynaptic NMDA receptor activation, and synaptic loss
Maria Talantova,Sara Sanz-Blasco,Xiaofei Zhang,Peng Xia,Mohd Waseem Akhtar,Shu-ichi Okamoto,Gustavo Dziewczapolski,Tomohiro Nakamura,Gang Cao,Alexander E. Pratt,Alexander E. Pratt,Yeon-Joo Kang,Shichun Tu,Elena Molokanova,Scott R. McKercher,Samuel Andrew Hires,Hagit Sason,David G. Stouffer,Matthew W. Buczynski,James P. Solomon,Sarah Michael,Evan T. Powers,Jeffery W. Kelly,Amanda J. Roberts,Gary Tong,Traci Fang-Newmeyer,James C. Parker,Emily A. Holland,Dongxian Zhang,Nobuki Nakanishi,H.-S. Vincent Chen,Herman Wolosker,Yuqiang Wang,Loren H. Parsons,Rajesh Ambasudhan,Eliezer Masliah,Stephen F. Heinemann,Juan C. Piña-Crespo,Stuart A. Lipton +38 more
TL;DR: The improved eNMDAR antagonist NitroMemantine, which selectively inhibits extrasynaptic over physiological synaptic NMDAR activity, protects synapses from Aβ-induced damage both in vitro and in vivo.