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Journal of Immunology (Baltimore, Md. : 1950)
|
February 15, 1987
Modulation of FcR function by complement: subcomponent C1q enhances the phagocytosis of IgG-opsonized targets by human monocytes and culture-derived macrophages
D A Bobak, T A Gaither, M M Frank, et al.
Journal of Immunology (Baltimore, Md. : 1950)
|
May 15, 1994
beta-Amyloid activates complement by binding to a specific region of the collagen-like domain of the C1q A chain
H Jiang, D Burdick, C G Glabe, et al.
Experimental Neurology
|
June 12, 1999
The presence of isoaspartic acid in beta-amyloid plaques indicates plaque age
M I Fonseca, E Head, P Velazquez, et al.
Immunity
|
February 1, 1997
cDNA cloning and primary structure analysis of C1qR(P), the human C1q/MBL/SPA receptor that mediates enhanced phagocytosis in vitro
R R Nepomuceno, A H Henschen-Edman, W H Burgess, et al.
Neuroreport
|
January 14, 1998
Complement activation by cross-linked truncated and chimeric full-length beta-amyloid
D H Cribbs, P Velazquez, B Soreghan, et al.
Experimental Neurology
|
March 1, 1996
Localization and cell association of C1q in Alzheimer's disease brain
A Afagh, B J Cummings, D H Cribbs, et al.
The Journal of Clinical Investigation
|
December 1, 1989
Human mannose-binding protein activates the alternative complement pathway and enhances serum bactericidal activity on a mannose-rich isolate of Salmonella
J E Schweinle, R A Ezekowitz, A J Tenner, et al.
Journal of Immunology (Baltimore, Md. : 1950)
|
May 25, 1991
Complement subcomponent C1q stimulates Ig production by human B lymphocytes
K R Young, J L Ambrus, A Malbran, et al.
Journal of Leukocyte Biology
|
November 8, 2001
C1qR(P), a myeloid cell receptor in blood, is predominantly expressed on endothelial cells in human tissue
M I Fonseca, P M Carpenter, M Park, et al.
Neurobiology of Disease
|
April 13, 2001
Complement association with neurons and beta-amyloid deposition in the brains of aged individuals with Down Syndrome
E Head, B Y Azizeh, I T Lott, et al.
Page
of 7
Search research articles
Search
Showing results (41-50 of 66) with videos related to
Sort By:
Page
of 7
Journal of Immunology (Baltimore, Md. : 1950)
|
February 15, 1987
Modulation of FcR function by complement: subcomponent C1q enhances the phagocytosis of IgG-opsonized targets by human monocytes and culture-derived macrophages
D A Bobak, T A Gaither, M M Frank, et al.
Journal of Immunology (Baltimore, Md. : 1950)
|
May 15, 1994
beta-Amyloid activates complement by binding to a specific region of the collagen-like domain of the C1q A chain
H Jiang, D Burdick, C G Glabe, et al.
Experimental Neurology
|
June 12, 1999
The presence of isoaspartic acid in beta-amyloid plaques indicates plaque age
M I Fonseca, E Head, P Velazquez, et al.
Immunity
|
February 1, 1997
cDNA cloning and primary structure analysis of C1qR(P), the human C1q/MBL/SPA receptor that mediates enhanced phagocytosis in vitro
R R Nepomuceno, A H Henschen-Edman, W H Burgess, et al.
Neuroreport
|
January 14, 1998
Complement activation by cross-linked truncated and chimeric full-length beta-amyloid
D H Cribbs, P Velazquez, B Soreghan, et al.
Experimental Neurology
|
March 1, 1996
Localization and cell association of C1q in Alzheimer's disease brain
A Afagh, B J Cummings, D H Cribbs, et al.
The Journal of Clinical Investigation
|
December 1, 1989
Human mannose-binding protein activates the alternative complement pathway and enhances serum bactericidal activity on a mannose-rich isolate of Salmonella
J E Schweinle, R A Ezekowitz, A J Tenner, et al.
Journal of Immunology (Baltimore, Md. : 1950)
|
May 25, 1991
Complement subcomponent C1q stimulates Ig production by human B lymphocytes
K R Young, J L Ambrus, A Malbran, et al.
Journal of Leukocyte Biology
|
November 8, 2001
C1qR(P), a myeloid cell receptor in blood, is predominantly expressed on endothelial cells in human tissue
M I Fonseca, P M Carpenter, M Park, et al.
Neurobiology of Disease
|
April 13, 2001
Complement association with neurons and beta-amyloid deposition in the brains of aged individuals with Down Syndrome
E Head, B Y Azizeh, I T Lott, et al.
Page
of 7