SPOP Antibody
- Known as:
- SPOP Antibody
- Catalog number:
- XW-7900
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- SPOP Antibody
Related genes to: SPOP Antibody
- Gene:
- SPOP NIH gene
- Name:
- speckle type BTB/POZ protein
- Previous symbol:
- -
- Synonyms:
- TEF2, BTBD32
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-07
- Date modifiied:
- 2016-02-10
Related products to: SPOP Antibody
Related articles to: SPOP Antibody
- In this issue of Molecular Cell, Cuneo et al. propose an equilibrium between two quaternary states of SPOP that can become dysregulated in cancer. SPOP oligomers form inactive double donuts or active linear filaments, as seen in gain-of-function cancer mutations. - Source: PubMed
Glennie LorraineHuang Danny T - The incidence of early-onset prostate cancer (EOPC) is rising, and by 2045 a 24.5% increase in cases and a 50% rise in mortality are projected. Accumulating evidence indicates that EOPC represents a distinct disease entity, characterized by unique molecular features, risk factor profiles, and clinical behavior that differ from standard-onset prostate cancer (SOPC). Nevertheless, research in this field remains nascent, and no consensus exists regarding the optimal management of EOPC. We synthesize current evidence on the epidemiology, molecular pathology, clinicopathological characteristics, survival, management, and early detection of EOPC. EOPC exhibits a distinctive molecular landscape, with TMPRSS2-ERG fusions occurring in 63-90% of cases as a hallmark alteration, whereas mutations in PTEN, SPOP, and CHD1 are significantly less frequent. Notably, the prevailing focus on hereditary EOPC has inadvertently led to the neglect of sporadic cases, which dominate clinical practice. Although localized EOPC confers no significant prognostic advantage over SOPC, high-risk or metastatic early-onset disease substantially elevates prostate-cancer-specific mortality. By critically appraising the existing evidence, we identify key knowledge gaps, such as the understudied sporadic EOPC subgroup and the lack of dedicated clinical trials, and propose future research directions to inform early detection and optimize therapeutic strategies for this unique patient population. - Source: PubMed
Publication date: 2026/07/22
Xiong XingyuZhu WeizhenHuang WeichaoZhang ShiyuDeng QiYang JieXu HangWei QiangYang Lu - Liquid biopsies using cell-free DNA (cfDNA) can identify actionable somatic alterations in prostate cancer (PCa). The presence of alterations related to clonal hematopoiesis (CH) can complicate interpretation of cfDNA results and lead to clinical inaction. We sought to determine alteration profiles identified by cfDNA testing in a large, racially diverse cohort of United States Veterans with metastatic PCa and quantify the extent of CH interference in the identification of actionable alterations. - Source: PubMed
Valle Luca FScobie MicaelaRowe KerryPritchard Colin CMontgomery BruceGarraway Isla PNickols Nicholas GSchoen Martin WKishan Amar UKelley Michael JRettig Matthew BMaxwell Kara N - Patient-derived organoids (PDOs) have transformed translational cancer research, allowing tractable models that better represent clinical features than traditional immortalized cell lines. Here we describe two PDOs with differential responses to carboplatin derived from sequential ascites fluid collections from a patient with high-grade müllerian carcinoma, that could not be further subclassified on the omental biopsy. Uterine origin was clinically excluded by pelvic imaging/CT scan of the uterus and absence of vaginal bleeding. Successful derivation from independent collections enabled comparison of intra-patient heterogeneity across sequential ascites samples and demonstrates that PDO efficiency rate is at least partly patient-specific or tumor-dependent. We performed long-read whole genome sequencing on the two PDOs, OC104 and OC109, to better characterize the structural variant landscape while also obtaining information on single nucleotide variants and DNA methylation. In addition to confirming single nucleotide variants noted in clinical sequencing (TP53, KRAS, SPOP, PPP2R1A, KMT2D), we identified additional variants in TSC2, NCOR2, and CTNNA2 that are predicted to be likely pathogenic. The spectrum of mutations, particularly the coincident KRAS and TP53, highlighted unexpected overlap with ovarian mucinous carcinoma. We also identified larger insertions and deletions that result in non-synonymous variants in MUC5AC, TPRX1, and BMX, as well as four translocation events, including two that could not have been resolved with short-read sequencing. Differentially methylated promoters between the two PDOs include 201 oncogenes and tumor suppressor genes, with HNF1A, MSI2, and SETBP1 having methylation directions consistent with these genes' roles in platinum response differences observed between the PDOs. Notably, the clonal nature of PDOs produced from two samples taken one week apart is important for the field to appreciate, particularly since they have clonal differences in platinum response. The temporal differences in clonality may indicate a limitation of low volume sampling, however may provide opportunity to longitudinally predict clinical outcomes. We also demonstrate the ability of long-read sequencing to add detail into the genomics and epigenetics of ovarian cancer. - Source: PubMed
Publication date: 2026/07/10
Wendt Jae RimAdams Kristin MMoreno RyanHossan Md ShahadatStram AustinLin Ethan SKersten LaurenKratz Jeremy DRoy MadhuchhandaMcGregor Stephanie MLang Jessica D - Speckle-type POZ protein (SPOP), a substrate receptor for the Cullin-3-RING (CRL3) ubiquitin ligase, is mutated in different cancers. Both activating and inactivating mutations in SPOP drive oncogenesis, underscoring the need for precise regulation. Among substrate receptors, SPOP uniquely assembles into filaments that are multivalent for substrate binding. Conversely, many substrates contain multiple SPOP-binding motifs. How this unusual reciprocal multivalent architecture regulates ubiquitination and how mutations activate SPOP are unclear. Gain-of-function mechanisms are also generally poorly understood. Here, we reveal that SPOP assemblies exist in an equilibrium between an active filament and a large, autoinhibited, circular "double-donut" state. Activating mutations shift the equilibrium, resulting in aberrant substrate turnover. Combinations of activating and inactivating mutations can produce intermediate activities, thus uncovering a tunable regulatory axis with implications for targeted cancer therapies. Therefore, SPOP's ability to assemble into long filaments is required for its regulation in human cells and underlies a gain-of-function mechanism. - Source: PubMed
Publication date: 2026/07/13
Cuneo Matthew JGüllülü ÖmerAmmar Mohamed-RaafetGui XinruiChurion KellyTurk MartinO'Flynn Brian GSabri NafisehMittag Tanja