RECK
Reversion-inducing cysteine-rich protein with Kazal motifs
Also known as: hRECK, RECK_HUMAN, ST15
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- O95980
- Gene
- RECK
- Ensembl
- ENSG00000122707
- Chromosome
- 9
- Canonical length
- 971 aa
- Protein class
- Plasma proteins, Predicted membrane proteins
- Subcellular location
- Plasma membrane
OverviewNCBI Gene
The protein encoded by this gene is a cysteine-rich, extracellular protein with protease inhibitor-like domains whose expression is suppressed strongly in many tumors and cells transformed by various kinds of oncogenes. In normal cells, this membrane-anchored glycoprotein may serve as a negative regulator for matrix metalloproteinase-9, a key enzyme involved in tumor invasion and metastasis. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Oct 2015]
Canonical amino-acid sequenceUniProt
971 residues, UniProt reviewed canonical sequence.
>O95980|RECK
1 MATVRASLRG ALLLLLAVAG VAEVAGGLAP GSAGALCCNH SKDNQMCRDV CEQIFSSKSE
61 SRLKHLLQRA PDYCPETMVE IWNCMNSSLP GVFKKSDGWV GLGCCELAIA LECRQACKQA
121 SSKNDISKVC RKEYENALFS CISRNEMGSV CCSYAGHHTN CREYCQAIFR TDSSPGPSQI
181 KAVENYCASI SPQLIHCVNN YTQSYPMRNP TDSLYCCDRA EDHACQNACK RILMSKKTEM
241 EIVDGLIEGC KTQPLPQDPL WQCFLESSQS VHPGVTVHPP PSTGLDGAKL HCCSKANTST
301 CRELCTKLYS MSWGNTQSWQ EFDRFCEYNP VEVSMLTCLA DVREPCQLGC RNLTYCTNFN
361 NRPTELFRSC NAQSDQGAMN DMKLWEKGSI KMPFINIPVL DIKKCQPEMW KAIACSLQIK
421 PCHSKSRGSI ICKSDCVEIL KKCGDQNKFP EDHTAESICE LLSPTDDLKN CIPLDTYLRP
481 STLGNIVEEV THPCNPNPCP ANELCEVNRK GCPSGDPCLP YFCVQGCKLG EASDFIVRQG
541 TLIQVPSSAG EVGCYKICSC GQSGLLENCM EMHCIDLQKS CIVGGKRKSH GTSFSIDCNV
601 CSCFAGNLVC STRLCLSEHS SEDDRRTFTG LPCNCADQFV PVCGQNGRTY PSACIARCVG
661 LQDHQFEFGS CMSKDPCNPN PCQKNQRCIP KPQVCLTTFD KFGCSQYECV PRQLACDQVQ
721 DPVCDTDHME HNNLCTLYQR GKSLSYKGPC QPFCRATEPV CGHNGETYSS VCAAYSDRVA
781 VDYYGDCQAV GVLSEHSSVA ECASVKCPSL LAAGCKPIIP PGACCPLCAG MLRVLFDKEK
841 LDTIAKVTNK KPITVLEILQ KIRMHVSVPQ CDVFGYFSIE SEIVILIIPV DHYPKALQIE
901 ACNKEAEKIE SLINSDSPTL ASHVPLSALI ISQVQVSSSV PSAGVRARPS CHSLLLPLSL
961 GLALHLLWTY NLocalizationUniProt · AlphaFold · HPA
Whether an antibody against RECK can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Cell surface
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.31
- Highest tissue expression
- 17 nTPM
Expression across tissuesHPA
Tissue
- ovary: 17 nTPM
- blood vessel: 15 nTPM
- tongue: 15 nTPM
- cervix: 14 nTPM
- adipose tissue: 14 nTPM
- smooth muscle: 14 nTPM
Single-cell type
- fibro-adipogenic progenitors: 155 nCPM
- microglia: 153 nCPM
- early primary spermatocytes: 138 nCPM
- oligodendrocytes: 137 nCPM
- breast lactating cells: 123 nCPM
- brain excitatory neurons: 118 nCPM
Immune cell
- naive CD4 T-cell: 6.3 nTPM
- memory CD4 T-cell: 5.2 nTPM
- non-classical monocyte: 4.8 nTPM
- naive CD8 T-cell: 4.6 nTPM
- MAIT T-cell: 4.5 nTPM
- memory CD8 T-cell: 4.2 nTPM
Brain region
- hippocampal formation: 9.7 nTPM
- cerebral cortex: 8.2 nTPM
- white matter: 8.2 nTPM
- medulla oblongata: 7.6 nTPM
- pons: 7.4 nTPM
- thalamus: 7.4 nTPM
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 0.67
- gnomAD pLI
- 0
- gnomAD missense Z
- 1.54
- DepMap mean gene effect
- -0.05
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- blood vessel maturation
- canonical Wnt signaling pathway
- embryo implantation
- embryonic forelimb morphogenesis
- extracellular matrix organization
- negative regulation of cell migration
- negative regulation of extracellular matrix disassembly
- positive regulation of canonical Wnt signaling pathway
- regulation of angiogenesis
- regulation of canonical Wnt signaling pathway
- regulation of establishment of blood-brain barrier
- regulation of extracellular matrix organization
- sprouting angiogenesis
Molecular functions
- coreceptor activity
- endopeptidase inhibitor activity
- metalloendopeptidase inhibitor activity
- serine-type endopeptidase inhibitor activity
- Wnt-protein binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Kazal domain
- Kazal domain superfamily
- Kazal-type serine protease inhibitor domain
- Reversion-inducing cysteine-rich protein with Kazal motifs
- Reversion-inducing cysteine-rich with Kazal motifs, N-terminal
- RECK, EGF-like 2 domain
- Reversion-inducing cysteine-rich protein with Kazal, EGF-like 1 domain
- Reversion-inducing cysteine-rich protein with Kazal, fibronectin type I module
- Reversion-inducing cysteine-rich protein with Kazal, CC4 domain
- Reversion-inducing cysteine-rich protein with Kazal, frizzled-like domain
- RECK-like, EGF-like 1 domain
- Reversion-inducing cysteine-rich with Kazal motifs, N-terminal
- RECK, frizzled-like domain
- RECK-like, CC4 domain
- RECK-like, EGF-like 1 domain
- RECK, fibronectin type I module
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of RECK in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads RECK as an antibody target. Whether an autoantibody or antibody against RECK could matter depends on whether native RECK is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
RECK is annotated at the cell surface, where native RECK is exposed to circulating antibodies and is a prime autoantibody target that could block, deplete, or overstimulate it.
Annotation status
The present source text does not explicitly label RECK as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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