- KCTD11 (17p13.1)
- https://www.ncbi.nlm.nih.gov/gene/147040
- Also known as
- REN; KCASH1; C17orf36; REN/KCTD11
- Preferred Names
- BTB/POZ domain-containing protein KCTD11
- Names
- RING-type E3 ubiquitin transferase subunit KCTD11
- potassium channel tetramerization domain-containing protein 11
- Retinoic acid, EGF, NGF induced gene protein
ORIGIN
1 mlgamfragt pmppnlnsqg gghyfidrdg kafrhilnfl rlgrldlprg ygetallrae
61 adfyqirpll dalreleasq gtpaptaall hadvdvsprl vhfsarrgph hyelssvqvd
121 tfranlfctd seclgalrar fgvasgdrae gsphfhlewa prpvelpeve ygrlglqplw
181 tggpgerrev vgtpsfleev lrvalehgfr ldsvfpdped llnsrslrfv rh
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KCTD11 tumor suppressor gene expression is reduced in prostate adenocarcinoma.
Zazzeroni F, et al. Biomed Res Int, 2014. PMID 25045667, Free PMC Article
-
Molecular organization of the cullin E3 ligase adaptor KCTD11.
Correale S, et al. Biochimie, 2011 Apr. PMID 21237243
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The tumor suppressor gene KCTD11REN is regulated by Sp1 and methylation and its expression is reduced in tumors.
Mancarelli MM, et al. Mol Cancer, 2010 Jun 30. PMID 20591193, Free PMC Article
-
Cullin 3 Recognition Is Not a Universal Property among KCTD Proteins.
Smaldone G, et al. PLoS One, 2015. PMID 25974686, Free PMC Article
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REN(KCTD11) is a suppressor of Hedgehog signaling and is deleted in human medulloblastoma.
Di Marcotullio L, et al. Proc Natl Acad Sci U S A, 2004 Jul 20. PMID 15249678, Free PMC Article
What's a GeneRIF?
-
Our
study demonstrates and supports that KCTD11, as well as negatively
regulated downstream effectors belonging to Hh signaling, plays a role
in prostate cancer pathogenesis.
-
the
protein is expressed in two alternative variants: a short previously
characterized form (sKCTD11) composed by 232 amino acids and a longer
variant (lKCTD11) which contains an N-terminal extension of 39 residues.
-
findings
identify KCTD11 as a widely down-regulated gene in human cancers, and
provide a basis to understand how its expression might be deregulated in
tumor cells
-
Results
identify REN(KCTD11) as a suppressor of Hedgehog signaling and suggest
that its inactivation might lead to a deregulation of the
tumor-promoting Hedgehog pathway in medulloblastoma.
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