Selected-GenAtlas references	SOURCE	GeneCards	NCBI Gene	Swiss-Prot	Ensembl
	HGNC	UniGene	Nucleotide	OMIM	UCSC

Home Page

FLASH GENE

Symbol

RHOC

contributors: mct/npt/pgu - updated : 14-06-2017

HGNC name	ras homolog gene family, member C
HGNC id	669

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

Location	1p13.1      Physical location : 113.243.748 - 113.250.025
Synonym name	Rho-related GTP-binding protein RhoC
	oncogene RHO H9
	small GTP binding protein RhoC
Synonym symbol(s)	RHOH9, ARH9, ARHC, MGC61427, MGC1448, H9

DNA

TYPE	functioning gene
STRUCTURE	6.28 kb     6 Exon(s)

MAPPING

cloned

Y

linked

N

status

provisional

RNA

TRANSCRIPTS	type	messenger

text	all transcripts encode the same protein

identification nb exons type bp product Protein kDa AA specific expression Year Pubmed NM_175744 6 - 1415 NP_786886 - 193 - 2009 19477269 NM_001042679 6 - 1313 NP_001036144 - 193 - 2009 19477269 NM_001042678 5 - 1346 NP_001036143 - 193 - 2009 19477269

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 Cardiovascular vessel         Digestive intestine small intestine         intestine large intestine colon       liver         Nervous brain         Skin/Tegument skin       predominantly Urinary kidney

tissue

System Tissue Tissue level 1 Tissue level 2 Level Pubmed Species Stage Rna symbol Connective bone

cell lineage

cell lines

fluid/secretion

at STAGE

physiological period

pregnancy

Text

placenta

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains

conjugated

LipoP

HOMOLOGY

interspecies

homolog to Aplysia Ras-related C

Homologene

FAMILY	small GTPase superfamily
	Rho family

CATEGORY

regulatory , protooncogene , signaling

SUBCELLULAR LOCALIZATION

plasma membrane

basic FUNCTION	GTPase, GTP binding protein (signal transduction)
	coordinated assembly of focal adhesions and stress fibers
	linking growth factor receptors to the activation of actin polymerization
	with RHOA, are essential for tumor invasion and/or metastasis in breast carcinomas
	playing a critical role in muscle differentiation
	mediating the distinct actin cytoskeleton
	changes required for both cellular motility and cell-cell adhesion
	responsible for stress fibre formation and inhibiting its expression reduces EMT-induced migration
	RHOA, RHOB and RHOC all have the potential to interact with the same downstream effectors, yet they have substantially different effects on cell shape and migratory properties

CELLULAR PROCESS	cell life, differentiation

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

signal transduction

a component

INTERACTION

DNA

RNA

small molecule	nucleotide,
	GTP

protein	putative regulator of myogenin and MEF25 genes
	actin
	potential binding partner for RHOC (LNX1, LNX2 and RHOC might be part of a larger protein complex that would have important functions in signaling transduction about regulating the transcriptional activities of AP-1)
	RHOC promotes polarized migration through FMNL3 by restricting lamellipodial broadening (
	RHOA and RHOC are both required for the ROCKent promotion of centrosome duplication
	RHOC, and RAC1 are essential, for IGFBP1-induced extravillous trophoblast (EVT migration
	PKN3 physically interacts with Rho-family GTPases, and preferentially with RHOC, a known mediator of tumor invasion and metastasis in epithelial cancers
	ARHGAP21 presented GAP activity for RHOA and RHOC and induced changes in cell morphology

cell & other

REGULATION

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function tumoral     --over   in metastatic melanoma tumoral     --over   Rho enhances the in vitro migration and invasion of melanocells

Susceptibility

Variant & Polymorphism

Candidate gene
Marker
Therapy target
	System Type Disorder Pubmed cancer     PKN3-RHOC complex represents an attractive therapeutic target in late-stage malignancies

ANIMAL & CELL MODELS