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FLASH GENE

Symbol

KLC1

contributors: shn/npt - updated : 03-10-2017

HGNC name	kinesin light chain 1
HGNC id	6387

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

EXPRESSION

Type	ubiquitous

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 Cardiovascular heart       moderately Lymphoid/Immune spleen       lowly Nervous brain       highly Reproductive male system testis     lowly Respiratory lung       specific Urinary kidney       lowly Visual eye       predominantly

tissue

System Tissue Tissue level 1 Tissue level 2 Level Pubmed Species Stage Rna symbol Muscular striatum skeletal   lowly

cell lineage

cell lines

fluid/secretion

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	N terminus with heptad repeats typical of the rod domain of cytoskeletal proteins
	six tetratricopeptide repeat (TPR)
	a central and C terminal consisting of 27 repeats of approximately 21 amino-acids, mediating binding to cargoes

mono polymer

tetramer

HOMOLOGY

interspecies	ortholog to Klc1, Mus musculus
	ortholog to Klc1, Rattus norvegicus
	ortholog to klc1, Danio rerio
	ortholog to KLC1, Pan troglodytes

Homologene

FAMILY

kinesin light chain family

CATEGORY

motor/contractile , transport carrier

SUBCELLULAR LOCALIZATION	intracellular
	intracellular,cytoplasm,organelle,Golgi
	intracellular,cytoplasm,cytoskeleton,microtubule
text	specific for the Golgi complex (Gyoeva 2000)

basic FUNCTION	may be playing a role in organelle transport
	light chain may function in coupling of cargo to the heavy chain or in the modulation of its ATPase activity
	involved in dendritic and axonal transport in the brain, is affected during chronic morphine treatment and may be involved in the development of opioid addiction (Bilecki 2009)
	complex of KLC1, KIF5C and CRMP2 is involved in transporting tubulin heterodimers and oligomers to the tip of the growing axon
	KLC1 may potentially compete with MAP1LC3A, a key component for autophagosome formation, to interact with FUNDC1

CELLULAR PROCESS	cell cycle, division

PHYSIOLOGICAL PROCESS

cellular trafficking transport

text	transport of organelles

PATHWAY

metabolism

signaling

a component

component of a complex with two kinesins, heavy chain and two light chains (KIF5A, KIF5B, KLC2, KLC1) (Morton 2010)

INTERACTION

DNA

RNA

small molecule

protein	kinesin family member 5C (KIF5C) and collapsin response mediator protein 2 (CRMP2)
	mitogen-activated protein kinase 8 interacting protein 3, MAPK8IP3(
	amyloid precursor protein, APP (
	SNAP25 and SNAP23 (
	JNK-interacting protein 1, JIP1 (
	sperm associated antigen 9, SPAG9 (
	caytaxin binds to KLC1 and functions as an adaptor that mediates intracellular transport of specific cargos, one of which is the mitochondrion
	cytoplasmic amino N-terminal domain of FUNDC1 is essential for interaction with KLC1

cell & other

REGULATION

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function constitutional       loss of function leading to axonal transport defects and gain of function of MAPT can initiate neurodegeneration and/or exacerbate human tau-dependent disease pathways in AD and other neurodegenerative tauopathies

Susceptibility

to Alzheimer disease to multiple scerosis (MS)

Variant & Polymorphism other	polymorphisms increasing the risk of Alzheimer disease
	56836CC variant proved to exert a significant protective effect on the occurrence of MS (Szolnoki 2007)

Candidate gene

Marker

Therapy target

ANIMAL & CELL MODELS

	KLC1 gene-targeted mice results in significantly smaller mutant mice that also exhibited pronounced motor disabilities (
	in living mice carrying a deletion of the kinesin light chain 1 (KLC1&
	8722;/&
	8722;) motor subunit revealed delayed axonal transport rates, and t early and selective transport defects can activate c-Jun N-terminal stress kinase (JNK) pathways that initiate abnormal hyperphosphorylation of tau in the absence of Abeta toxicity (
	mislocalization of opsin is a major cause of photoreceptor cell death from kinesin-2 dysfunction (