Discover Community Create You

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

LRP5 competes for SPOP binding to enhance tumorigenesis mediated by Daxx and PD-L1 in prostate cancer.

Experimental cell research - 1 Jan 2024

Gan Sishun, Qu Fajun, Zhang Xiangmin, Pan Xiuwu, Xu Da, Cui Xingang, Hou Jianquan

Abstract excerpt

Genetic factors coordinate with environmental factors to drive the pathogenesis of prostate adenocarcinoma (PRAD). SPOP is one of the most mutated genes and LRP5 mediates lipid metabolism that is abnormally altered in PRAD. Here, we investigated the potential cross-talk between SPOP and LRP5 in PRAD. We find a negative correlation between SPOP and LRP5 proteins in PRAD. SPOP knockdown increased LRP5 protein while...

Read the complete abstract on PubMed

Topics

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

Share to B7-H1 Antigen
Share to Carcinogenesis
Share to Cell Transformation, Neoplastic

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Co-Repressor Proteins

Share to Low Density Lipoprotein Receptor-Related Protein-5

Share to Molecular Chaperones

Share to Prostatic Neoplasms

Share to Repressor Proteins

Source

Identifiers

PMID: 38008278
DOI: 10.1016/j.yexcr.2023.113857

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

LRP5 competes for SPOP binding to enhance tumorigenesis mediated by Daxx and PD-L1 in prostate cancer.PMID 38008278Read ↗

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

ERK1/2 inhibits Cullin 3/SPOP-mediated PrLZ ubiquitination and degradation to modulate prostate cancer progression.Semantic proximity Read ↗

Phosphorylation-dependent regulation of SPOP by LIMK2 promotes castration-resistant prostate cancer.Semantic proximity Read ↗

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

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

Androgen receptor is the key transcriptional mediator of the tumor suppressor SPOP in prostate cancer.Semantic proximity Read ↗

Prostate Cancer-associated SPOP mutations enhance cancer cell survival and docetaxel resistance by upregulating Caprin1-dependent stress granule assembly.Semantic proximity Read ↗

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

Parkinson’s Disease as a Risk Factor for Prostate Adenocarcinoma: A Molecular Point of ViewSemantic proximity Read ↗

Dysregulation of INF2-mediated mitochondrial fission in SPOP-mutated prostate cancer.Semantic proximity Read ↗

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