LRP12 antibody
- Known as:
- LRP12 (anti-)
- Catalog number:
- orb100320
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- LRP12 antibody
Related genes to: LRP12 antibody
- Gene:
- LRP12 NIH gene
- Name:
- LDL receptor related protein 12
- Previous symbol:
- -
- Synonyms:
- ST7, FLJ12929
- Chromosome:
- 8q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-06
- Date modifiied:
- 2016-10-05
Related products to: LRP12 antibody
Related articles to: LRP12 antibody
- KRAS G12C-mutated non-small cell lung carcinoma (NSCLC), caused by a glycine-to-cysteine substitution at codon 12, is associated with poor prognosis and is now targetable with specific inhibitors. We retrospectively analyzed 279 KRAS G12C-mutated NSCLC cases (2017-2023) from our registry with available histologic, immunohistochemical, and molecular data. The cohort included 279 patients (125 females, 151 males; mean age 67 years, range 29-91). Most tumors were primary lung carcinomas (n = 229, 82%), while 45 (16%) were metastatic at presentation. Morphologic evaluation was available in 240 tumors: 37% showed solid squamous cell carcinoma (SCC)-like features, 61% rhabdoid/plasmacytoid morphology, and 17% sarcomatoid features. Adenocarcinoma-associated patterns were present in 67 cases, often mixed, and focal solid growth occurred in 77%. TTF1, Napsin A, and CK7 were positive in 86%, 87%, and 98%, respectively, whereas squamous markers were infrequent (p40/p63 7%, CK5/6 8%). PD-L1 expression was detected in 65%. Co-mutations most commonly involved TP53 (n = 27) and STK11 (n = 12); IDH1/2, PIK3CA, and CTNNB1 mutations occurred in four cases each, MET in two cases, and BRAF, FGFR2, FGFR3, and GNAS in one case each. Two gene fusions were identified (LRP12::NRG1, FGFR3::TACC3). Mean survival was 1.89 years, with one- and five-year survival rates of 54% and 25%. KRAS G12C-mutated NSCLC is clinically aggressive and frequently shows solid growth with rhabdoid, plasmacytoid, or SCC-like morphology, which may lead to misclassification and missed genetic testing. Immunohistochemistry and molecular profiling are essential for accurate classification and enabling targeted therapy. - Source: PubMed
Publication date: 2026/04/15
Bradová MartinaSlavík PetrVaněček TomášMartínek PetrGrossmann PetrKormunda StanislavBehenská KristýnaSvatoň MartinPešek MilošJirásek Tomᚊpůrková ZuzanaHroudová PetraMrázková HanaHořavová BarboraRoubec JaromírBaník MartinMukenšnábl PetrMichal MichalŠvajdler Marián - Oculopharyngodistal myopathy (OPDM) is a hereditary muscle disease caused by CGG/CCG repeat expansions in six genes. Although the clinical features are often similar, such as ptosis, dysphagia, and distal muscle weakness, the age at onset vary widely, and the mechanisms underlying this variation remain unclear. In particular, the contributions of repeat size, flanking sequence variation, and DNA methylation to phenotype have not been systematically explored using single-molecule resolution. - Source: PubMed
Publication date: 2026/03/27
Eura NobuyukiNoguchi SatoruOgawa MegumuSonehara KyutoYamanaka AiKurashige TakashiHayashi ShinichiroOkada YukinoriSugie KazumaNishino Ichizo - Oculopharyngodistal myopathy (OPDM) is characterized by ptosis, ophthalmoparesis, dysphagia, and distal weakness. Myopathological features include rimmed vacuoles and intranuclear inclusions. OPDM is associated with a pathogenic CGG repeat expansions in the 5'UTR of LRP12, NOTCH2NLC, GIPC1, RILPL1 and ABCD3. Translation of the repeat in the glycine reading frame has been demonstrated for expansions in FMR1, NOTCH2NLC and GIPC1. To assess for a similar phenomenon with LRP12, we expressed normal or expanded CGG repeats in the context of the 5'UTR of LRP12, upstream of a green fluorescent protein (GFP) in the three repeat reading frames. Repeat dependent translation occurs exclusively in the glycine reading frame. However, unlike other CGG repeat disorders, there is no proximal AUG, or near-AUG cognate initiated polyglycine (polyG) open reading frame in LRP12. Instead, our results support a model in which repeat-associated non-AUG (RAN) mediated polyG translation may initiate within the arginine reading frame and then undergo a + 1 translational frameshift into the glycine reading frame. LRP12-associated polyG products form intranuclear SQSTM1/ubiquitin positive inclusions that are cytotoxic and alter the nuclear lamina architecture in transfected cells. While FMR1-associated polyG inclusions are cytosolic, LRP12-associated polyG inclusions are nuclear in transfected skeletal muscle. LRP12 expansion carrier iPSC derived myotubes exhibit SQSTM1 positive intra- and peri- nuclear inclusions when compared with control patient myotubes, suggesting that polyG expression can occur in patients. Together, these findings provide evidence of RAN translation and polyG-toxicity in LRP12-associated OPDM pathology. - Source: PubMed
Publication date: 2026/03/06
Li ChengchengDaw Jil APittman Sara KMaltby Connor JSakurai HidetoshiTodd Peter KWeihl Conrad C - Acute myeloid leukemia (AML) is a highly heterogeneous hematological malignancy with a poor prognosis, thus necessitating novel prognostic biomarkers and therapeutic targets. This study investigated the role of long non-coding RNAs (lncRNAs) in the pathogenesis and risk stratification of AML. Transcriptome sequencing was conducted on bone marrow samples from 20 patients with AML (10 low/intermediate-risk and 10 high-risk), revealing 344 differentially expressed lncRNAs and 1,109 dysregulated mRNAs. The application of functional enrichment analysis revealed that NF-κB signaling activation and Th17 cell differentiation represent the key pathways associated with high-risk AML. Among dysregulated lncRNAs, RNase P RNA Component H1 (RPPH1) demonstrated significant upregulation in patients with high-risk AML, thus establishing it as a promising candidate for further investigation. Functional validation employing AML cell lines MV-4-11 and MOLM13 demonstrated that RPPH1 overexpression enhanced cell proliferation and suppressed apoptosis, whereas its knockdown resulted in opposite effects. Mechanistically, RPPH1 enhanced NF-κB p65 phosphorylation and upregulated IL-17 A expression, thereby activating downstream oncogenic targets, including PLAC8, LRP12, and CRABP2. The present findings suggest that RPPH1 regulates AML progression via the NF-κB/Th17A signaling axis, providing new insights into its role in disease pathogenesis and immune microenvironment remodeling. In view of its prognostic and therapeutic potential, RPPH1 can function as both a biomarker and a promising therapeutic target for high-risk AML. - Source: PubMed
Publication date: 2025/12/01
Wang ManqingLi WenluLuo CongCao YixiongLu ZhongweiZhu JiaqiXiang MeiLiao PeiLi Junjun - Tumor-associated inflammation and macrophage polarization drive gastric cancer (GC) progression. We aimed to identify inflammation-related biomarkers that predict prognosis and modulate the tumor immune microenvironment, focusing on LDL receptor-related protein 12 (LRP12). We integrated public datasets with an in-house cohort to build an immune-related prognostic model based on inflammatory response-related genes (IRRGs) and to nominate candidate genes. Single-cell transcriptomics were used to map cell-type enrichment. Key findings were validated by multiplex immunofluorescence/immunohistochemistry, LRP12 overexpression and knockdown in GC cell lines, in vitro proliferation and invasion assays, western blotting for signaling pathways, and xenograft models. LRP12 was identified as a differentially expressed IRRG-associated gene and emerged as a robust prognostic marker, enriched in malignant cells and macrophage populations. High LRP12 expression correlated with poorer overall survival and with M2 macrophage markers (CD163, CD206). Functional studies using both overexpression and knockdown showed that LRP12 promotes GC cell proliferation and invasion, while xenografts of LRP12-knockdown cells exhibited reduced tumor growth. Mechanistically, LRP12 overexpression activated the AKT/mTOR pathway, reflected by increased phosphorylation of AKT and mTOR. LRP12-associated signatures were linked to an immunosuppressive microenvironment characterized by M2 macrophage infiltration and may indicate responsiveness to therapies that repolarize M2-like tumor-associated macrophages. LRP12 is a prognostic biomarker in GC that promotes tumor progression via AKT/mTOR signaling and M2 macrophage-mediated immunosuppression, with potential to inform personalized therapeutic strategies. - Source: PubMed
Publication date: 2025/11/23
Wang YufeiYin XinWang MeiDingZhu MengXue Yingwei