Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Dysregulation of INF2-mediated mitochondrial fission in SPOP-mutated prostate cancer.

PLoS genetics - 1 Apr 2017

Jin Xiaofeng, Wang Jie, Gao Kun, Zhang Pingzhao, Yao Longfang, Tang Yan, Tang Lisha, Ma Jian, Xiao Jiantao, Zhang Enceng, Zhu Jie, Zhang Bin, Zhao Shi-Min, Li Yao, Ren Shancheng, Huang Haojie, Yu Long, Wang Chenji

Abstract excerpt

Next-generation sequencing of the exome and genome of prostate cancers has identified numerous genetic alternations. SPOP (Speckle-type POZ Protein) was one of the most frequently mutated genes in primary prostate cancer, suggesting SPOP is a potential driver of prostate cancer development and progression. However, how SPOP mutations contribute to prostate cancer pathogenesis remains poorly understood. SPOP acts...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Dynamins
Share to Formins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to GTP Phosphohydrolases

Share to Microfilament Proteins

Share to Microtubule-Associated Proteins

Share to Mitochondrial Dynamics

Share to Mitochondrial Proteins

Share to Neoplasm Invasiveness

Source

Open in PubMed Open full text

Identifiers

PMID: 28448495
DOI: 10.1371/journal.pgen.1006748
PMCID: PMC5426793

Genes

SPOP
INF2
CUL3
RBX1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Dysregulation of INF2-mediated mitochondrial fission in SPOP-mutated prostate cancer.PMID 28448495Read ↗

SPOP promotes ATF2 ubiquitination and degradation to suppress prostate cancer progressionSemantic proximity Read ↗

Destruction of DDIT3/CHOP protein by wild-type SPOP but not prostate cancer-associated mutants.Semantic proximity Read ↗

SPOP mutations promote p62/SQSTM1-dependent autophagy and Nrf2 activation in prostate cancer.Semantic proximity Read ↗

Enhanced autophagy and NFE2L2/NRF2 pathway activation in SPOP mutation-driven prostate cancer.Semantic proximity Read ↗

SPOP Gene Mutations in Prostate Cancer: Deciphering Their Role in Disease Characterization and Targeted Interventions on AR SignalingSemantic proximity Read ↗

G3BP1 inhibits Cul3SPOP to amplify AR signaling and promote prostate cancer.Semantic proximity Read ↗

Prostate cancer-associated mutation in SPOP impairs its ability to target Cdc20 for poly-ubiquitination and degradation.Semantic proximity Read ↗

SPOP-mediated ubiquitination and degradation of PDK1 suppresses AKT kinase activity and oncogenic functions.Semantic proximity Read ↗

Prostate cancer. Ubiquitylome analysis identifies dysregulation of effector substrates in SPOP-mutant prostate cancer.Semantic proximity Read ↗

SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor-Induced Growth Suppression.Semantic proximity Read ↗

Dual functions of SPOP and ERG dictate androgen therapy responses in prostate cancer.Semantic proximity Read ↗

Deregulation of SPOP in Cancer.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.