FAM123B antibody
- Known as:
- FAM123B (anti-)
- Catalog number:
- orb101291
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- FAM123B antibody
Related genes to: FAM123B antibody
- Gene:
- AMER1 NIH gene
- Name:
- APC membrane recruitment protein 1
- Previous symbol:
- FAM123B
- Synonyms:
- RP11-403E24.2, FLJ39827, WTX
- Chromosome:
- Xq11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-07-11
- Date modifiied:
- 2019-04-23
Related products to: FAM123B antibody
Related articles to: FAM123B antibody
- - Source: PubMed
Publication date: 2026/08/13
Szmyd BartoszPodstawka MałgorzataPastorczak AgataMłynarski WojciechJaskólski Dariusz JWiśniewski Karol - While classical tumor suppressors in colorectal cancer (CRC) are predominantly recognized for restraining cell-autonomous proliferation, their extrinsic mandate in orchestrating the tumor immunometabolic niche remains poorly defined. Clinically, we document that APC membrane recruitment protein 1 (AMER1) downregulation correlates with advanced progression and cytotoxic CD8 T cell spatial exclusion in CRC patients. Using parallel homograft models in diverse host immune backgrounds, we show that tumoral AMER1 confers robust in vivo tumor-suppressive effects that are dependent on a fully functional immune system. Single-cell RNA sequencing reveals that tumoral AMER1 enrichment actively preserves CD8 T cell effector stemness by expanding the CXCR5 precursor exhausted subset (Tpex) across regional lymph nodes and primary tumor microenvironments. Integrated multi-omics and biochemical tracking identify dopamine (DA) as the conserved neurometabolic effector driving this niche remodeling. Mechanistically, AMER1 physically binds and rescues dopa decarboxylase (DDC) from post-translational degradation to sustain tumoral DA secretion; conversely, AMER1 loss creates a localized DA void. Cell-autonomously, tumoral DA accumulation triggers gasdermin D (GSDMD)-dependent tumor pyroptosis. Therapeutically, local DA administration halts multi-lineage carcinoma progression by reversing CD8 T cell terminal exhaustion and reinforcing central memory differentiation. Collectively, our findings redefine AMER1 as a critical immunometabolic gatekeeper and establish neurotransmitter metabolic bypassing as a promising therapeutic strategy for CRC. - Source: PubMed
Publication date: 2026/08/03
Dang Jun LongHu QiLu YangWang JieLi XiaoxueChen YixiongZhao JunLiu YuWang JulieZang NiankeZhou LiZhong XiaolanLi WanglinZheng Song Guo - Early-onset colorectal cancer (EOCRC) is increasing disproportionately among Hispanic/Latino (H/L) populations and demonstrates substantial molecular and clinical heterogeneity. Although Wingless/Integrated (WNT) pathway alterations are among the most common genomic events in colorectal cancer, their prognostic significance in the context of contemporary systemic therapies, including Bevacizumab, remains incompletely understood. We conducted an integrative clinical-genomic analysis of colorectal cancer cohorts stratified by age at diagnosis, ancestry, and Bevacizumab exposure, interrogating somatic alterations across curated WNT signaling pathway genes. Conversational artificial intelligence agents (AI-HOPE and AI-HOPE-WNT) enabled dynamic cohort construction, treatment-specific subgroup analyses, and pathway-level interrogation through natural language-driven clinical-genomic integration. WNT pathway alterations, predominantly involving APC, were highly prevalent across all cohorts; however, their distribution and clinical associations demonstrated strong treatment-, ancestry-, and age-dependent variability. Bevacizumab-treated tumors exhibited lower mutation frequencies in several WNT regulators, including RNF43, AXIN1/2, TCF7L2, and AMER1, suggesting potential biologic interaction or treatment-related selective pressure. Importantly, WNT pathway alterations were associated with improved overall survival in H/L EOCRC and Non-Hispanic White (NHW) late-onset colorectal cancer, but with worse survival in NHW EOCRC, highlighting distinct ancestry- and age-specific prognostic effects. These findings support the role of the WNT pathway dysregulation as a disparity-aware biomarker framework in colorectal cancer and demonstrate the utility of conversational AI systems for scalable multidimensional clinical-genomic integration in precision oncology. - Source: PubMed
Publication date: 2026/07/11
Ruiz-Garcia ErikaWaldrup BrigetteCarranza Francisco GManjarrez SophiaFernandez-Figueroa Edith AVelazquez-Villarreal Enrique - Molecular biomarkers are increasingly used for risk stratification, particularly in up-front surgery settings (Children's Oncology Group trials), whereas in preoperative chemotherapy setting, the ongoing International Society of Pediatric Oncology (SIOP)-Renal Tumor Study Group-2016 UMBRELLA study aims to validate selected biomarkers for future risk-adapted treatment strategies. This systematic review summarizes all literature on the prognostic value of these biomarkers. - Source: PubMed
Publication date: 2026/05/18
Oller AgustinaKemmeren PatrickPerotti Danielavan Tinteren HarmVerschuur ArnauldSpreafico FilippoBrok JesperFurtwängler Rhoikos C JChowdhury TanzinaAl-Saadi ReemVujanic Gordan MTreece Amy LDrost Jarnovan Grotel MartineMullen Elizabeth AEvageliou Nicholas FGraf NorbertHong Andrew LGessler ManfredGeller James Ivan den Heuvel-Eibrink Marry M - Osteopathia striata with cranial sclerosis (OSCS) is a rare X-linked dominant genetic disorder mediated by variants in the AMER1 gene, characterized primarily by generalized skeletal sclerosis and striated changes. However, research on its craniofacial phenotypes has long been fragmented, lacking systematic pedigree construction and basis for precise management. This study integrates a 16-year follow-up patient carrying a novel AMER1 frameshift variant (c.966delT; p.Phe322Leufs*3) with 66 literature-confirmed patients, and systematically analyzes craniofacial phenotypic characteristics and genetic associations using Spearman correlation analysis, two-step clustering, and gene function prediction. The results show that orofacial clefts have the highest incidence (72%), with synergistic associations between retained deciduous teeth and impacted permanent teeth; two-step clustering identified four heterogeneous "genetic abnormality-phenotype" subtypes, with DNA/protein functional status as the core factor; it confirms that c.966delT is a pathogenic de novo variant, mediating Wnt pathway abnormalities as the core mechanism of phenotypes, and proposes a multidisciplinary management strategy. This study is the first to establish a quantitative pedigree and subtype classification for OSCS craniofacial phenotypes, deepening the understanding of molecular mechanisms and providing key basis for precise diagnosis, stratified intervention, and prognosis improvement. - Source: PubMed
Publication date: 2026/04/10
Chen QingWang XinLiu NiankeYuan WenjunSong Yaling