WWOX (Phospho-Tyr33) Antibody
- Known as:
- WWOX (Phospho-Tyr33) Antibody
- Catalog number:
- 11779
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- WWOX (Phospho-Tyr33) Antibody
Related genes to: WWOX (Phospho-Tyr33) Antibody
- Gene:
- WWOX NIH gene
- Name:
- WW domain containing oxidoreductase
- Previous symbol:
- -
- Synonyms:
- FOR, WOX1, SDR41C1
- Chromosome:
- 16q23.1-q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-31
- Date modifiied:
- 2018-02-13
Related products to: WWOX (Phospho-Tyr33) Antibody
Related articles to: WWOX (Phospho-Tyr33) Antibody
- Genomic alterations have been reported to correlate with patients' response to immune checkpoint inhibitor (ICI) therapy in hepatocellular carcinoma (HCC). The present study aimed to examine whether single nucleotide polymorphism (SNP) is associated with ICI treatment-related side effects and progression-free survival (PFS) in HCC patients. - Source: PubMed
Publication date: 2026/06/10
Lin Po-TingTeng WeiChen Wei-TingChu Yu-DeSu Chung-WeiHsieh Yi-ChungLin Chen-ChunLin Yung-ChangLin Chun-YenYeh Chau-TingLin Shi-Ming - Chemoresistance is a primary factor limiting nasopharyngeal carcinoma (NPC) treatment. Growing evidence indicates that E3 ubiquitin ligases play a pivotal role in chemoresistance. Here, we identified that the E3 ubiquitin ligase RNF138 is significantly upregulated in NPC patients who do not respond to chemotherapy. Our study reveals that RNF138 promotes the K48-linked ubiquitination of hnRNPA0 at K133, thereby destabilizing WWOX mRNA. The subsequent loss of WWOX protein relieves the inhibition of JAK2 self-phosphorylation, leading to constitutive pathway activation. Consequently, RNF138-JAK2/STAT3 activation suppresses chemotherapy-induced apoptosis via reduced ROS production and promotes immune evasion by upregulating PD-L1. Clinically, high RNF138 expression correlated with poor prognosis and resistance to chemotherapy. In conclusion, this study unveils the RNF138-hnRNPA0-WWOX axis as a driver of JAK2/STAT3 activation, leading to both chemoresistance and immune evasion in NPC. This work positions RNF138 as a valuable biomarker to guide individualized chemotherapy, and highlights JAK inhibitors as a potential targeted therapy for NPC patients. - Source: PubMed
Publication date: 2026/06/11
He ChuyuLou LimingLei YuanWen XianhuiHuang DaofengLai HaibinHuang JiachenZhou LeweiZhang QianqianMa JunLiang YelinQiao HanZhang Yuan - Limbic-predominant age-related TDP-43 encephalopathy neuropathologic change is a common proteinopathy in the oldest old that is associated with cognitive decline. Although the genetic basis of limbic-predominant age-related TDP-43 encephalopathy neuropathologic change remains largely unknown, , and loci are frequently implicated. Here, we examined nine previously reported limbic-predominant age-related TDP-43 encephalopathy neuropathologic change risk loci ( and ) in a population cohort of 262 individuals from the Vantaa 85 + study. We also tested whether Alzheimer's disease polygenic risk score without was associated with limbic-predominant age-related TDP-43 encephalopathy neuropathologic change. Using ordinal logistic regression models, rs5848 (odds ratio = 2.45, 95% confidence interval: 1.71-3.52, adjusted = 5.75 × 10), ε4 dose (odds ratio = 1.73, 95% confidence interval: 1.07-2.80, adjusted = 0.030) and rs72643142 (odds ratio = 2.38, 95% confidence interval: 1.38-4.11, adjusted = 0.0048) were associated with higher limbic-predominant age-related TDP-43 encephalopathy neuropathologic change stage. Additionally, Alzheimer's disease polygenic risk score without was associated with limbic-predominant age-related TDP-43 encephalopathy neuropathologic change after adjusting for age, sex, Alzheimer's disease pathology and ε4 dose (odds ratio = 1.36, 95% confidence interval: 1.06-1.75, adjusted = 0.027). Our findings contribute to the understanding of limbic-predominant age-related TDP-43 encephalopathy neuropathologic change genetics and suggest shared biological processes between limbic-predominant age-related TDP-43 encephalopathy neuropathologic change and Alzheimer's disease. - Source: PubMed
Publication date: 2026/05/28
Mikhailenko ElizavetaSavola SaraKero MiaTienari Pentti JMyllykangas LiisaKaivola Karri - - Source: PubMed
Sobczak MSawicz ZSzczerbal ISwitonski MNowacka-Woszuk J - The WW domain-containing oxidoreductase () gene, well-known as a tumor suppressor, also has a crucial role as a transcription factor in the developing brain. The bi-allelic loss of the gene causes a condition characterized by drug-resistant epilepsy, developmental delay, and neurological impairments, often resulting in mortality within the first year of life, known as -related epileptic encephalopathy (WOREE) syndrome (MIM: 616211). Whole Exome Sequencing (WES) analysis was performed on a female patient who died within three months of birth and was diagnosed with microcephaly, severe early-onset refractory seizures, and drug-resistant epileptic encephalopathy. WES revealed a 38 kb CNV deletion spanning exons 6-7, and a known frameshift variant in exon 8, impairing a highly clinically significant region of the encoded protein. Clinical and genetic features of reported WOREE patients with gene deletions similar to our patient were analyzed. Our case highlights the clinical heterogeneity of variants in WOREE syndrome and expands the spectrum of reported compound heterozygous deletions. Further research needs to elucidate pathophysiology and improve diagnostic and therapeutic strategies. - Source: PubMed
Publication date: 2026/04/25
Sapuppo AnnamariaRizzo RobertaFusto GaiaRocca RobertaSortino VincenzoPappalardo Xena GiadaRuggieri MartinoFalsaperla Raffaele