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FLASH GENE

Symbol

SFRP5

contributors: mct/npt - updated : 12-09-2016

HGNC name	secreted frizzled-related protein 5
HGNC id	10779

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

RNA

TRANSCRIPTS	type	messenger

identification nb exons type bp product Protein kDa AA specific expression Year Pubmed NM_003015 3 - 1883 NP_003006 35.4 317 - 2008 18795670

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 Endocrine pancreas       highly

tissue

System Tissue Tissue level 1 Tissue level 2 Level Pubmed Species Stage Rna symbol Epithelial barrier/lining       Nervous central

cell lineage

cell lines

fluid/secretion

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	frizzled-like cysteine-rich domain
	a conserved hydrophilic carboxyterminal domain

HOMOLOGY

interspecies	homolog to Drosophila frizzled polarity
	homolog to murine Sfrp 5

Homologene

FAMILY

secreted frizzled-related protein (sFRP) family

CATEGORY

signaling

SUBCELLULAR LOCALIZATION	extracellular
	plasma membrane

basic FUNCTION	likely involved in WNT binding and in determining the polarity of photoreceptors and other cells in retina
	in the setting of obesity, SFRP5 secretion by adipocytes exerts salutary effects on metabolic dysfunction by controlling inflammatory cells within adipose tissue (pMID: 20558665)
	may play a probable defensive role in impeding gastric cancer progression, characteristically by inhibiting gastric epithelial cells (GEC) migration induced by macrophage-derived WNT5A via JNK signaling activation
	cellular actions of SFRP5 seem to depend on the type of tissue as well as its inflammatory and metabolic state
	acts as a mature adipocyte marker but not as a regulator in adipogenesis
	is a negative regulator of glucose metabolism
	functions to antagonize inflammatory responses after ischemia/reperfusion (I/R) in the heart, possibly through a mechanism involving non-canonical WNT5A/JNK signaling
	possible detrimental role of SFRP5 for insulin secretion

CELLULAR PROCESS

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

signal transduction

a component

INTERACTION

DNA

RNA

small molecule

protein

IFT88 and primary cilia regulate expression of SFRP5 and WNT signaling pathways in growth plate via regulation of IHH signaling

cell & other

REGULATION

inhibited by

glucose (glucose inhibits likely SFRP5 expression via the PI3K/AKT pathway and hence promotes pancreatic beta-cell proliferation)

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function tumoral       loss of function in colorectal cancer by hypermethylation tumoral     --low   by hypermethylation in primary hepatocellular carcinoma (Takagi 2008) tumoral     --low   by hypermethylation in breast cancer associated with unfavorable prognosis (Veeck 2008) tumoral     --low   CpG methylation-dependent silencing was frequently seen in gastric cancer(Nojima 2007) constitutional     --over   inhibited early B-cell differentiation in the bone marrow (BM), resulting in the accumulation of cells with a common lymphoid progenitor (CLP) phenotype constitutional     --low   in obese children, especially in those with metabolic syndrome (MetS), and negatively correlated with body mass index (BMI)

Susceptibility

Variant & Polymorphism

Candidate gene	SFRP5 methylation may be a novel DNA-based biomarker potentially useful in clinical breast cancer management (Veeck 2008)
	DNA methylation markers of Gastric cancer (GC), which may serve as useful markers that may identify a distinct subset of GC (Kang 2008)
Marker	represents a candidate for a mature adipocyte marker gene
Therapy target

ANIMAL & CELL MODELS

	mice overexpressing Sfrp5 had fewer B-lymphocytes in the peripheral blood and spleen
	mice that lack functional Sfrp5 were resistant to diet-induced obesity
	Sfrp5-deficient mice fed a high-calorie diet developed severe glucose intolerance and hepatic steatosis, and their adipose tissue showed an accumulation of activated macrophages