Mouse polyclonal to SPRYD3, Host Mouse
- Known as:
- Mouse pab SPRYD3, Host Mouse
- Catalog number:
- YF-PA26753
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal SPRYD3 Host
Related genes to: Mouse polyclonal to SPRYD3, Host Mouse
- Gene:
- SPRYD3 NIH gene
- Name:
- SPRY domain containing 3
- Previous symbol:
- -
- Synonyms:
- FLJ14800
- Chromosome:
- 12q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2006-01-25
- Date modifiied:
- 2015-07-22
Related products to: Mouse polyclonal to SPRYD3, Host Mouse
Related articles to: Mouse polyclonal to SPRYD3, Host Mouse
- Head and neck squamous cell carcinoma (HNSCC) exhibits marked heterogeneity driven by both tumor-intrinsic programs and immune context. However, the relationship between epithelial proliferation and immune activity remains incompletely defined. - Source: PubMed
Publication date: 2026/07/01
He LimingZeng YiyuGao YijunXie XiaoyanLiu Yang - MYCBP2 (PAM) is a large signaling hub that plays a key role in various processes, including neuronal connectivity and growth, cell division, and protein ubiquitination. Together with the substrate specificity factor FBXO45, MYCBP2 forms an E3 ligase complex that is involved in mitotic cell fate decision. During extended mitotic arrest caused by anti-microtubule drugs, cells may either experience cell death or escape mitosis through mitotic slippage. E3 ligase mediated ubiquitination is antagonized by deubiquitinating enzymes (DUBs). In this study, we show that despite their opposing activities, DUB-E3 ligase complexes can form and cooperate. We identify an E3 ligase complex consisting of MYCBP2 and a new substrate specificity factor, SPRYD3. Interestingly, SPRYD3-MYCBP2 promotes bipolar spindle formation by facilitating non-canonical ubiquitination on the DUB USP11 cysteine 318. We find that this process promotes bipolar spindle formation and mitotic slippage in presence of microtubule targeting drugs. - Source: PubMed
Publication date: 2025/10/04
Turi da Fonte Dias Alexandra RitaHoffmann Ingrid - FKBP51, also known as FK506-binding protein 51, is a molecular chaperone and scaffolding protein with significant roles in regulating hormone signaling and responding to stress. Genetic variants in FKBP5, which encodes FKBP51, have been implicated in a growing number of neuropsychiatric disorders, which has spurred efforts to target FKBP51 therapeutically. However, the molecular mechanisms and sub-anatomical regions influenced by FKBP51 in these disorders are not fully understood. In this study, we aimed to examine the impact of Fkbp5 ablation using circadian phenotyping and molecular analyses. Our findings revealed that the lack of FKBP51 did not significantly alter circadian rhythms, as detected by wheel-running activity, but did offer protection against stress-mediated disruptions in rhythmicity in a sex-dependent manner. Protein changes in Fkbp5 KO mice, as measured by histology and proteomics, revealed alterations in a brain region- and sex-dependent manner. Notably, regardless of sex, aged Fkbp5 KOs showed elevated MYCBP2, FBXO45, and SPRYD3 levels, which are associated with neuronal-cell adhesion and synaptic integrity. Additionally, pathways such as serotonin receptor signaling and S100 family signaling were differentially regulated in Fkbp5 KO mice. Weighted protein correlation network analysis identified protein networks linked with synaptic transmission and neuroinflammation. The information generated by this work can be used to better understand the molecular changes in the brain during aging and in the absence of Fkbp5, which has implications for the continued development of FKBP51-focused therapeutics for stress-related disorders. - Source: PubMed
Publication date: 2024/09/03
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