Reply to Woodruff et al.: C1q and C3-dependent complement pathway activation does not contribute to disease in SOD1 mutant ALS mice

Proceedings of the National Academy of Sciences of the United States of America

Volumn 111, Issue 1, 2014, Pages

  Lobsiger, Christian S ^a,b,c,d   Cleveland, Don W ^d  

^a INSERM   (France)

^b CNRS   (France)

^c SORBONNE UNIVERSITÉ   (France)

^d UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

COMPLEMENT COMPONENT C1Q; COMPLEMENT COMPONENT C3; COMPLEMENT COMPONENT C5A; COMPLEMENT COMPONENT C5A RECEPTOR;

AMYOTROPHIC LATERAL SCLEROSIS; BLOOD CLOTTING; COMPLEMENT ACTIVATION; DISEASE COURSE; GENE DELETION; LETTER; MSOD1 MOUSE; NONHUMAN; PRIORITY JOURNAL; SURVIVAL;

AMYOTROPHIC LATERAL SCLEROSIS; ANIMALS; COMPLEMENT C1Q; COMPLEMENT PATHWAY, CLASSICAL; MOTOR NEURONS; SUPEROXIDE DISMUTASE;

EID: 84891955128     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.1321606111     Document Type: Letter

References (5)

1. Sarma JV, Ward PA (2011) The complement system. Cell Tissue Res 343(1): 227-235.
2. Lobsiger CS, et al. (2013) C1q induction and global complement pathway activation do not contribute to ALS toxicity in mutant SOD1 mice. Proc Natl Acad Sci USA 110(46): E4385-E4392.
3. Woodruff TM, Lee JD, Noakes PG (2014) Role for terminal complement activation in amyotrophic lateral sclerosis disease progression. Proc Natl Acad Sci USA 111: E3-E4.
4. Huber-Lang M, et al. (2006) Generation of C5a in the absence of C3: A new complement activation pathway. Nat Med 12(6): 682-687.
5. Lee JD, et al. (2013) Dysregulation of the complement cascade in the hSOD1G93A transgenic mouse model of amyotrophic lateral sclerosis. J Neuroinflammation 10(1):119.