YWHAB antibody
- Known as:
- YWHAB (anti-)
- Catalog number:
- orb129765
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- YWHAB antibody
Related genes to: YWHAB antibody
- Gene:
- YWHAB NIH gene
- Name:
- tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein beta
- Previous symbol:
- YWHAA
- Synonyms:
- -
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1993-09-20
- Date modifiied:
- 2016-10-05
Related products to: YWHAB antibody
Related articles to: YWHAB antibody
- Gut dysbiosis has been increasingly implicated in post-stroke cognitive impairment (PSCI); however, the causal contribution and therapeutic potential of gut microbiota-derived metabolites remain unclear. This study aimed to identify key microbiota-derived metabolites involved in PSCI and elucidate their underlying mechanisms. We found that both PSCI patients and middle cerebral artery occlusion (MCAO) mice exhibited distinct gut microbial alterations, characterized by a marked reduction in tryptophan-metabolizing bacteria and indole-3-propionic acid (IPA), a gut microbiota-derived tryptophan metabolite. Exogenous IPA administration alleviated PSCI-like phenotypes in MCAO mice. Mechanistically, IPA preserved tyrosine hydroxylase-positive (Th) fibers and catecholamine levels in the dorsal hippocampus. Further analyses showed that IPA binds to the adaptor protein Ywhab, promotes ERK activation, and enhances neuronal survival, thereby counteracting neuronal apoptosis-associated inflammation, and subsequent Th fiber degeneration. These findings identify IPA as a gut microbiota-derived neuromodulator that mitigates PSCI by preserving dorsal hippocampal catecholaminergic transmission. IPA may therefore serve as a therapeutic candidate for PSCI. - Source: PubMed
Publication date: 2026/10/07
Liu YisiZhang HuayingXia FangboGao XuxuanWu FanZhao XinLi MengxiZheng YanniYan SiqiXu KaiyuChen MuxuanRen YueranHu WeikeLi ZhuangYin JiaZhou HongweiZhang Dongxin - Early follicular development and primordial follicle formation are essential for ovarian reserve establishment, and disruption of this process may contribute to fertility disorders such as premature ovarian insufficiency (POI). Figla is an oocyte-specific transcription factor required for primordial follicle formation, but its candidate downstream genes and associated pathways remain incompletely understood. This study aimed to investigate the role of Figla in early follicular development and to explore its potential downstream regulatory events. A Figla knockout mouse model was generated to evaluate the effects of Figla deficiency on ovarian development and primordial follicle formation. ChIP-seq, motif analysis, and promoter activity assays were performed to identify FIGLA-associated chromatin regions and candidate genes. In addition, Figla overexpression and Ywhab knockdown experiments were conducted in a granulosa cell line, together with ovarian tissue Western blot analysis, to assess changes in growth activity, migration, ERK phosphorylation, and apoptosis-related markers. Figla was highly expressed in late embryonic and early postnatal ovaries, and its deletion primarily disrupted perinatal primordial follicle assembly, accompanied by progressive oocyte loss. ChIP-seq, motif, and promoter analyses supported Ywhab as a candidate gene potentially regulated by Figla. In KGN cells, Figla overexpression increased Ywhab expression and coincided with greater growth activity, migration, ERK phosphorylation, and changes in BAD/BCL-2/BAX-related markers. These cellular and signaling changes were attenuated by Ywhab knockdown. Additional ovarian tissue analysis showed reduced p-ERK/ERK and increased p-BAD/BAD ratios in Figla(-/-) ovaries. These findings support Ywhab as a candidate downstream gene potentially regulated by Figla and suggest a possible link between Figla-associated transcriptional regulation and cellular processes relevant to early follicular development. Further validation is needed before extending these findings to ovarian reserve establishment more broadly or to POI-related reproductive disorders. - Source: PubMed
Publication date: 2026/10/06
Yang LeLi LinshuangShen LinZhang Hanwang - YWHA/14-3-3 proteins are conserved phosphoserine/phosphothreonine-binding adaptors that coordinate signaling-complex assembly, subcellular localization, stress responses and cell-state transitions. Although often discussed as a single adaptor family, colorectal cancer (CRC) studies suggest that individual YWHA isoforms act through distinct clients, RNA-associated layers and tumor-state contexts. In this narrative and mechanistic review, we synthesized PubMed-indexed CRC literature through 18 May 2026 and appraised CRC-relevant mechanistic modules using an explicit evidence-maturity rubric developed by the authors distinct from formal GRADE assessment. We propose an isoform-client-context framework for interpreting 14-3-3 biology in CRC. YWHAG has been linked to CTTN-dependent Wnt/β-catenin activation, whereas YWHAE/14-3-3ϵ protein has been associated with extracellular-vesicle secretion and EV-associated β-catenin/Wnt outputs. Separately, the YWHAE-encoded lncRNA, hereafter referred to as YWHAE lncRNA, has been proposed to activate KRAS/ERK and PI3K/AKT signaling through a competing endogenous RNA mechanism. YWHAZ participates in epithelial-mesenchymal and G2/M transitions through miR-1-3p- and TRIP13-associated mechanisms. YWHAB supports PIK3R2-dependent PI3K/AKT signaling, whereas YWHAH connects NAT10/ac4C regulation, CD8+ T-cell exhaustion and MAPK/ERK-dependent autophagy-associated invasion. SFN illustrates context-dependent tumor-suppressive or stress-adaptive functions. Overall, total 14-3-3 abundance is insufficient for mechanistic or translational interpretation. Interactomics, phosphoproteomics, spatial profiling, extracellular-vesicle analysis and patient-derived models should be used to prioritize YWHA-dependent candidate mechanisms for functional validation. These modules should currently be regarded as testable biomarker and therapeutic hypotheses, not as clinically validated CRC biomarkers or targets. - Source: PubMed
Publication date: 2026/08/19
Liu QianLi RudongYe WeiZhao Zhipeng - Oxidative stress is closely involved in osteoarthritis (OA), but the cell-type-specific oxidative stress landscape and related regulatory molecules in human cartilage remain incompletely defined. This study aimed to identify effector chondrocyte (EC)-associated oxidative stress features in OA and to prioritize candidate molecules linked to p47phox-NOX2-related ROS responses. - Source: PubMed
Publication date: 2026/08/07
Yuan ShuaiChen HuirunWei JiaxueTan JinxianLiu ShuaiFu Zhenyang - Alzheimer's disease (AD) plasma and cerebrospinal fluid (CSF) proteomics can distinguish AD from cognitively normal controls, but the generalizability of machine learning performance and the recurrence of biological signals across datasets require cautious interpretation. We developed an explainable artificial intelligence framework spanning two fluids and four ADNI proteomic datasets, covering 2082 modality specific samples, all analysed internally within ADNI. Phase 1 analysed plasma using a 119 analyte NULISA and targeted UPENN panel (n = 727; 216 CE, 511 controls). Phase 2 extended the analysis to CSF using SOMAscan7k, TMT-MS and targeted SET2, with Elecsys Aβ42, Aβ40, total tau and p-tau181 as anchor biomarkers. Only SOMAscan was subject-independent relative to Phase 1 plasma; TMT-MS and SET2 overlapped with Phase 1 for 96.0% and 97.7% of subjects and therefore are not independent replication cohorts. Under subject-level splits with fold internal preprocessing, we compared Elastic Net, Explainable Boosting Machines and gradient boosted trees with SHAP-based explanations. Among the candidate pipelines, we selected the pipeline with the highest held-out test ROC AUC for each platform; the selected values were 0.927 in plasma and 0.954-0.973 across the three CSF datasets. Because the same held out test performance was used for pipeline selection and headline reporting, these are optimistically selected single-holdout estimates, not unbiased estimates of generalizable or clinical performance. Explanations identified five recurring biological axes within ADNI: cholinergic (ACHE), tau/14-3-3 (YWHAG, YWHAZ, YWHAB, YWHAE), neuro-axonal (NEFL, NEFH), microglial/complement (CHIT1, SMOC1, CHI3L1, C7, CFH) and synaptic (NPTXR, NPTX2, DLG4, SYT5, VSNL1, ELAVL2). CSF analyses showed synaptic vesicle-cycle enrichment (q = 2 × 10), and CSF YWHAG correlated strongly with total tau (ρ = 0.87). Cross-fluid directional concordance was modest overall (54-57%) but increased to 73-80% among mapped analyte/protein rows reaching q < 0.05 in CSF. These findings provide hypothesis-generating, internally supported evidence within ADNI. Independent external cohorts with locked pipelines are required to evaluate generalizable performance and biological reproducibility; the overlapping TMT-MS and SET2 analyses should not be interpreted as independent replication. - Source: PubMed
Publication date: 2026/06/15
Donmez Turker BerkMansour Mohammed