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FLASH GENE

Symbol

C5

contributors: mct/npt - updated : 02-05-2013

HGNC name	complement component 5
HGNC id	1331

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

EXPRESSION

Type

expressed in	(based on citations)
organ(s)	System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Digestive liver         Lymphoid/Immune tonsils         Nervous brain diencephalon hypothalamus

tissue

System Tissue Tissue level 1 Tissue level 2 Level Pubmed Species Stage Rna symbol Blood / hematopoietic bone marrow

cell lineage
cell lines
fluid/secretion	plasma

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	one anaphylatoxin-like domain
	one NTR domain

secondary structure

an alpha 2

conjugated

GlycoP

isoforms

Precursor

HOMOLOGY

interspecies	ortholog to murine Hc
	ortholog to rattus c5

Homologene

FAMILY

CATEGORY

immunity/defense

SUBCELLULAR LOCALIZATION	extracellular
	plasma membrane
	intracellular
	intracellular,cytoplasm

basic FUNCTION	complement component 5, initiating, after activation, the assembly of the late complement components C5-C9 into the membrane attack complex
	activation of the complement cascade and formation of C5a may play a role in the onset of acute coronary events by induction of MMPs in atherosclerotic lesions (
	its activation elicits proteolytic cascades which eventually results in the cleavage of the C5 protein into two fragments, C5a and C5b

CELLULAR PROCESS

cell communication

PHYSIOLOGICAL PROCESS

immunity/defense , inflammation

text	chemotaxis C5a

PATHWAY

metabolism

signaling

signal transduction

a component

component 5 associating with the late components to form the membrane attack complex

INTERACTION

DNA

RNA

small molecule

protein	C5b, the C345C domain of C5 and the FIMs of C7, which mediates reversible binding of C5 to C7 in solution, plays an essential role in MAC (membrane attack complex) formation and complement lytic activity
	thrombin and C5 convertase are invariant partners, enhancing the terminal pathway via the generation of newly uncovered C5 intermediates
	small anaphylatoxin C5a induces a variety of biological responses upon binding to the 7TM receptors C5aR and the C5L2, while the large C5b fragment nucleates formation of the membrane attack complex capable of killing susceptible pathogens by the formation of a pore structure

cell & other

REGULATION

inhibited by

inactivated (cleaved) in the classical pathway by the complex C4b,C2a,C3b and in the alternative pathway by the complex C3b,BF

ASSOCIATED DISORDERS

corresponding disease(s)

C5

related resource

C5base - Mutation registry for C5 deficiency

Susceptibility

to hepatic fibrosis to rheumatoid arthritis to adverse cardiovascular outcome in male patients with carotid atherosclerosis

Variant & Polymorphism other	a common genetic variant at the TRAF1-C5 locus is associated with an increased risk of anti-CCP-positive rheumatoid arthritis (Plenge 2007)
	C5 rs17611 GG genotype is associated with increased C5a plasma levels and represents a risk factor for adverse cardiovascular outcome in male patients with carotid atherosclerosis

Candidate gene
Marker	C5 fragment levels in cerebrospinal fluid (CSF) of patients with bacterial meningitis correlated with several clinical indicators of poor prognosis
Therapy target
	System Type Disorder Pubmed immunology infectious   C5-specific monoclonal antibodies could be a promising new antiinflammatory adjuvant therapy for pneumococcal meningitis

ANIMAL & CELL MODELS

C5a receptor-deficient mice with pneumococcal meningitis had lower CSF wbc counts and decreased brain damage compared with WT mice