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Speckle-type POZ protein

SPOP, speckle-type POZ protein, TEF-2
This gene encodes a protein that may modulate the transcriptional repression activities of death-associated protein 6 (DAXX), which interacts with histone deacetylase, core histones, and other histone-associated proteins. In mouse, the encoded protein binds to the putative leucine zipper domain of macroH2A1.2, a variant H2A histone that is enriched on inactivated X chromosomes. The BTB/POZ domain of this protein has been shown in other proteins to mediate transcriptional repression and to interact with components of histone deacetylase co-repressor complexes. Alternative splicing of this gene results in multiple transcript variants encoding the same protein. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Ubiquitin, Cul3, CAN, Cullin, Gli
Papers on SPOP
Two paths for stabilization of ERG in prostate carcinogenesis: TMPRSS2-ERG fusions and speckle-type pox virus and zinc finger protein mutations.
Wang et al., Pittsburgh, United States. In Asian J Androl, Feb 2016
UNASSIGNED: Speckle-type POZ (pox virus and zinc finger protein) protein (SPOP) is an E3 ubiquitin ligase adaptor protein that specifically promotes the ubiquitination and proteasome degradation of proteins.
SPOP E3 Ubiquitin Ligase Adaptor Promotes Cellular Senescence by Degrading the SENP7 deSUMOylase.
Zhang et al., Philadelphia, United States. In Cell Rep, Dec 2015
The SPOP gene, which encodes an E3 ubiquitin ligase adaptor, is frequently mutated in a number of cancer types.
The Molecular Taxonomy of Primary Prostate Cancer.
Cancer Genome Atlas Research Network et al., In Cell, Dec 2015
Our results revealed a molecular taxonomy in which 74% of these tumors fell into one of seven subtypes defined by specific gene fusions (ERG, ETV1/4, and FLI1) or mutations (SPOP, FOXA1, and IDH1).
Next-generation sequencing technology in prostate cancer diagnosis, prognosis, and personalized treatment.
Tewari et al., New York City, United States. In Urol Oncol, Jun 2015
New recurrent alterations have been identified in PCa (e.g., TMPRSS2-ERG translocation, SPOP and CHD1 mutations, and chromoplexy), and many previous ones in well-established pathways have been validated (e.g., androgen receptor overexpression and mutations; PTEN, RB1, and TP53 loss/mutations).
Reprint of: The prostate cancer genome: Perspectives and potential.
Tomlins et al., Ann Arbor, United States. In Urol Oncol, Feb 2015
Lesions more specific to prostate cancer include alterations in androgen signaling, gene fusions of ETS transcription factors, and mutations in SPOP.
Molecular foundations for personalized therapy in prostate cancer.
Cheng et al., Indianapolis, United States. In Curr Drug Targets, 2014
Lastly, we briefly discuss emerging genetic subtypes defined by either SPINK1 overexpression, CHD1 inactivation, or SPOP mutations.
Identification and Validation of Novel Hedgehog-Responsive Enhancers Predicted by Computational Analysis of Ci/Gli Binding Site Density.
Gumucio et al., Ann Arbor, United States. In Plos One, 2014
Of the 22 Ci/Gli clusters tested, seven novel enhancers (and the previously known patched enhancer) were identified as Hh-responsive and Ci/Gli-dependent in one or both of these assays, including: Cuticular protein 100A (Cpr100A); invected (inv), which encodes an engrailed-related transcription factor expressed at the anterior/posterior wing disc boundary; roadkill (rdx), the fly homolog of vertebrate Spop; the segment polarity gene gooseberry (gsb); and two previously untested regions of the Hh receptor-encoding patched (ptc) gene.
Tumor suppressor SPOP mediates the proteasomal degradation of progesterone receptors (PRs) in breast cancer cells.
Wang et al., Shanghai, China. In Am J Cancer Res, 2014
Speckle-type POZ protein (SPOP) is an adaptor protein of the CUL3-based E3 ubiquitin ligase complexes.
Prostate cancer. Ubiquitylome analysis identifies dysregulation of effector substrates in SPOP-mutant prostate cancer.
Garraway et al., Cambridge, United States. In Science, 2014
Here, we analyzed changes in the ubiquitin landscape induced by prostate cancer-associated mutations of SPOP, an E3 ubiquitin ligase substrate-binding protein.
The emerging role of speckle-type POZ protein (SPOP) in cancer development.
Mani, Dallas, United States. In Drug Discov Today, 2014
Speckle-type POZ (pox virus and zinc finger protein) protein (SPOP) is an E3 ubiquitin ligase adaptor protein that is frequently mutated in prostate and endometrial cancers.
The prostate cancer genome: perspectives and potential.
Tomlins et al., Ann Arbor, United States. In Urol Oncol, 2014
Lesions more specific to prostate cancer include alterations in androgen signaling, gene fusions of ETS transcription factors, and mutations in SPOP.
Exome sequencing of serous endometrial tumors identifies recurrent somatic mutations in chromatin-remodeling and ubiquitin ligase complex genes.
Bell et al., Bethesda, United States. In Nat Genet, 2012
We identified high frequencies of somatic mutations in CHD4 (17%), EP300 (8%), ARID1A (6%), TSPYL2 (6%), FBXW7 (29%), SPOP (8%), MAP3K4 (6%) and ABCC9 (6%).
Adaptor protein self-assembly drives the control of a cullin-RING ubiquitin ligase.
Privé et al., Toronto, Canada. In Structure, 2012
Adaptor protein self-assembly provides a graded level of regulation of the SPOP/Cul3 E3 ligase toward its multiple protein substrates.
Exome sequencing identifies recurrent SPOP, FOXA1 and MED12 mutations in prostate cancer.
Garraway et al., New York City, United States. In Nat Genet, 2012
SPOP was the most frequently mutated gene, with mutations involving the SPOP substrate-binding cleft in 6-15% of tumors across multiple independent cohorts.
Breast cancer metastasis suppressor 1 (BRMS1) is destabilized by the Cul3-SPOP E3 ubiquitin ligase complex.
Kim et al., Seoul, South Korea. In Biochem Biophys Res Commun, 2012
These results suggest that the novel regulatory mechanism of BRMS1 by Cul3-SPOP complex is important for breast cancer progression.
Tumor-suppressor role for the SPOP ubiquitin ligase in signal-dependent proteolysis of the oncogenic co-activator SRC-3/AIB1.
O'Malley et al., Houston, United States. In Oncogene, 2011
SPOP expression inhibited SRC-3-mediated oncogenic signaling and tumorigenesis.
Multiple Ser/Thr-rich degrons mediate the degradation of Ci/Gli by the Cul3-HIB/SPOP E3 ubiquitin ligase.
Jiang et al., Dallas, United States. In Proc Natl Acad Sci U S A, 2010
similar S/T-rich motifs are present in Gli proteins as well as in numerous HIB-interacting proteins and mediate Gli degradation by SPOP
Structures of SPOP-substrate complexes: insights into molecular architectures of BTB-Cul3 ubiquitin ligases.
Schulman et al., Memphis, United States. In Mol Cell, 2009
The study provides a molecular understanding of how SPOP and other MATH-BTB proteins recruit substrates to Cul3 and how their dimerization and conformational variability may facilitate avid interactions with diverse substrates.
Analysis of Drosophila segmentation network identifies a JNK pathway factor overexpressed in kidney cancer.
White et al., Chicago, United States. In Science, 2009
study found that SPOP plays a conserved role in TNF-mediated JNK signaling and was highly expressed in 99% of clear cell renal cell carcinomas
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