FAM89B antibody
- Known as:
- FAM89B (anti-)
- Catalog number:
- orb101722
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- FAM89B antibody
Related genes to: FAM89B antibody
- Gene:
- FAM89B NIH gene
- Name:
- family with sequence similarity 89 member B
- Previous symbol:
- -
- Synonyms:
- MTVR1, LRAP25
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-09-13
- Date modifiied:
- 2018-05-10
Related products to: FAM89B antibody
Related articles to: FAM89B antibody
- Glaucoma poses a significant global health challenge, yet reliable biomarkers for its diagnosis and treatment remain scarce. This study employed Mendelian randomization (MR) and bioinformatics approaches to identify potential biomarkers for glaucoma. Using the GSE9944 dataset, differentially expressed genes (DEGs) were identified and analyzed through protein-protein interaction (PPI) networks and functional enrichment. MR analysis selected DEGs for further evaluation using support vector machine-recursive feature elimination (SVM-RFE), with genes exhibiting high differential expression and an area under the curve (AUC) > 0.7 considered as candidate biomarkers. Among 836 DEGs, the PPI network revealed complex interactions, and functional enrichment highlighted significant involvement of the PI3K-AKT and MAPK signaling pathways. MR analysis linked 113 DEGs to glaucoma, with 57 genes showing consistent expression trends. SVM-RFE identified six signature genes, among which ATP6V0D1 and FAM89B emerged as robust biomarkers (AUC > 0.7). Molecular regulatory network analysis and drug prediction analysis further revealed potential mechanisms and compounds targeting these biomarkers, providing new therapeutic avenues for glaucoma. Experimental validation confirmed that ATP6V0D1 and FAM89B were significantly downregulated under both mechanical and swelling stress conditions, with concurrent suppression of the PI3K/AKT pathway. In conclusion, ATP6V0D1 and FAM89B are promising biomarkers for glaucoma, offering potential applications in diagnosis, treatment, and advancing the understanding of glaucoma pathogenesis. - Source: PubMed
Publication date: 2025/07/01
Lin XiuliMa ChuanyongZhang XiaoxueQiu YuzheCui YiXu Nuo - Animal studies have reinforced clinical reports of cognitive impairment in cancer survivors following chemotherapy but, until now, all pre-clinical research in this area has been conducted on normal rodents. The present study investigated the effects of chemotherapy on cognition and underlying biological mechanisms in the FVB/N-Tg (MMTV-neu) 202 Mul/J mouse, a well-characterized transgenic model of breast cancer that has similarities to the tumorigenesis which occurs in humans. Tumor-bearing and control mice received three weekly injections of a combination of methotrexate + 5-fluorouracil, or an equal volume of saline. Different aspects of learning and memory were measured before and after treatment. The effects of tumor and chemotherapy on neurogenesis, neuro-inflammatory cytokine activity, and brain volume, as they relate to corresponding cognitive changes, were also measured. The toxic effects of chemotherapy extended to the cancerous model in which substantial cognitive impairment was also associated with the disease. Cognitive deficits were greatest in tumorigenic mice that received the anti-cancer drugs. Both tumor growth and chemotherapy caused significant changes in brain volume, including the hippocampus and frontal lobes, two structures that are directly implicated in cognitive tasks that were shown to be vulnerable. The level of hippocampal neurogenesis in adulthood was suppressed in chemotherapy-treated mice and associated with loss of hippocampus-controlled cognitive function. Dysregulation of cytokine activity was found in tumorigenic mice and associated with impaired cognitive performance. The results show that chemotherapy and tumor development independently contribute to cognitive deficits through different biological mechanisms. - Source: PubMed
Publication date: 2017/11/04
Winocur GordonBerman HalNguyen MaryBinns Malcolm AHenkelman Markvan Eede MatthijsPiquette-Miller MichelineSekeres Melanie JWojtowicz J MartinYu JohnsonZhang HaiboTannock Ian F - A rate-limiting aspect of transgenic mouse models of mammary adenocarcinoma is that primary tumor burden in mammary tissue typically defines study end-points. Thus, studies focused on elucidating mechanisms of late-stage de novo metastasis are compromised, as are studies examining efficacy of anti-cancer therapies targeting mediators of metastasis in the adjuvant setting. Numerous murine mammary cancer models have been developed via targeted expression of dominant oncoproteins to mammary epithelial cells yielding models variably mimicking histopathologic and transcriptome-defined breast cancer subtypes common in women. While much has been learned regarding the biology of mammary carcinogenesis with these models, their utility in identifying molecules regulating growth of late-stage metastasis are compromised as mice are typically euthanized at earlier time points due to significant primary tumor burden. Moreover, since a significant percentage of women diagnosed with breast cancer receive adjuvant therapy after surgical resection of primary tumors and prior to presence of detectable metastatic disease, preclinical models of de novo metastasis are urgently needed as platforms to evaluate new therapies aimed at targeting metastatic foci. To address these deficiencies, we developed a murine model of de novo mammary cancer metastasis, wherein primary mammary tumors are surgically resected, and metastatic foci subsequently develop over a 115 day post-surgical period. This long latency provides a tractable model to identify functionally significant regulators of metastatic progression in mice lacking primary tumor, as well as a model to evaluate preclinical therapeutic efficacy of agents aimed at blocking functionally significant molecules aiding metastatic tumor survival and growth. - Source: PubMed
Publication date: 2017/07/29
Gast Charles EShaw Aubie KWong Melissa HCoussens Lisa M - Overexpression of the oncoprotein erbB2/HER2 is present in 20-30% of breast cancer patients and inversely correlates with patient survival. Reports have demonstrated the deterministic power of the mammary microenvironment where the normal mammary microenvironment redirects cells of non-mammary origin or tumor-derived cells to adopt a mammary phenotype in an in vivo model. This phenomenon is termed tumor cell redirection. Tumor-derived cells that overexpress the erbB2 oncoprotein lose their tumor-forming capacity in this model. In this model, phosphorylation of erbB2 is attenuated thus reducing the tumor cell's tumor-forming potential. In this report, we describe our results using an in vitro model based on the in vivo model mentioned previously. Tumor-derived cells are mixed in predetermined ratios with normal mammary epithelial cells prior to seeding in vitro. In this in vitro model, the tumor-derived cells are redirected as determined by attenuated phosphorylation of the receptor and reduced sphere and colony formation. These results match those observed in the in vivo model. This in vitro model will allow expanded experimental options in the future to determine additional aspects of tumor cell redirection that can be translated to other types of cancer. - Source: PubMed
Publication date: 2015/04/22
Park Jang PyoBlanding Walker MFeltracco Jessica ABooth Brian W - Myotonic dystrophy kinase-related Cdc42-binding kinase (MRCK) has been shown to localize to the lamella of mammalian cells through its interaction with an adaptor protein, leucine repeat adaptor protein 35a (LRAP35a), which links it with myosin 18A (MYO18A) for activation of the lamellar actomyosin network essential for cell migration. Here, we report the identification of another adaptor protein LRAP25 that mediates MRCK association with LIM kinase 1 (LIMK1). The lamellipodium-localized LRAP25-MRCK complex is essential for the regulation of local LIMK1 and its downstream F-actin regulatory factor cofilin. Functionally, inhibition of either MRCK or LRAP25 resulted in a marked suppression of LIMK1 activity and down-regulation of cofilin phosphorylation in response to aluminum fluoride induction in B16-F1 cells, which eventually resulted in deregulation of lamellipodial F-actin and reorganization of cytoskeletal structures causing defects in cell polarization and motility. These biochemical and functional characterizations thus underline the functional relevance of the LRAP25-MRCK complex in LIMK1-cofilin signaling and the importance of LRAP adaptors as key determinants of MRCK cellular localization and downstream specificities. - Source: PubMed
Publication date: 2014/08/08
Lee Irene Cheng JieLeung ThomasTan Ivan