Sheep Nucleoporin 50kDa ELISA kit
- Known as:
- Sheep Nucleoporin 50kDa Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- e14n0059
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Blue gene shanghai
- Gene target:
- Sheep Nucleoporin 50kDa ELISA kit
Ask about this productRelated genes to: Sheep Nucleoporin 50kDa ELISA kit
- Gene:
- LAMA3 NIH gene
- Name:
- laminin subunit alpha 3
- Previous symbol:
- LAMNA
- Synonyms:
- nicein-150kDa, kalinin-165kDa, BM600-150kDa, epiligrin
- Chromosome:
- 18q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-14
- Date modifiied:
- 2015-11-23
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- Cisplatin resistance is the principal cause of relapse in high-grade serous ovarian cancer (HGSOC), but bulk-expression signatures cannot localize resistant malignant states or the tumor-microenvironment (TME) interactions that sustain them. This study aimed to define cisplatin-resistant epithelial cell states and their regulatory and metabolic circuits by integrating multi-cohort single-cell transcriptomes with pharmacogenomic and clinical data. - Source: PubMed
Publication date: 2026/08/14
Jia ZhaoyangPan WenjingZhao XiboLi LianxiuTan Wenhua - Breast cancer is the leading cause of cancer-related mortality among women. Laminin subunit alpha 3 (LAMA3), a constituent of the extracellular matrix, is associated with tumor progression. However, its clinical relevance and function remain inadequately understood. - Source: PubMed
Publication date: 2026/08/04
Tan ZheqiongLiu SuotianZhao DanDu ShangSheng ChengfeiWang HuiLu Zhongxin - The coexistence of LOCS and a broader EB phenotype within a single consanguineous family represents a unique instance of intra-familial phenotypic heterogeneity in LAMA3-related junctional epidermolysis bullosa. This highlights the importance of recognizing systemic manifestations, including urological and neurological complications, and underscores early diagnosis, multidisciplinary management, and genetic counseling. - Source: PubMed
Publication date: 2026/08/02
Rasheed ZainabRashid MuhammadMahmud Usman SyedJavaid Muhammad HassaanMahato Raghabendra KumarYaqoob Zubaria - The laminin α3 chain, encoded by LAMA3, constitutes a principal component of laminin-332 (LN-332), an essential extracellular matrix (ECM) glycoprotein governing cell adhesion, proliferation, and tissue homeostasis. This systematic review consolidates current evidence on the molecular features and regulatory mechanisms of LAMA3, including its roles in PI3K/Akt, epithelial-mesenchymal transition (EMT), and Hippo-YAP signaling, as well as epigenetic and post-transcriptional modulation. Its context-dependent functions across distinct pathological states are delineated. In malignancies, including colorectal and ovarian cancers, LAMA3 functions as an oncogenic determinant that enhances invasion, metastatic dissemination, and chemotherapeutic resistance. In contrast, in hereditary diseases such as junctional epidermolysis bullosa (JEB) and chronic disorders such as idiopathic pulmonary fibrosis (IPF), LAMA3 deficiency or dysfunction constitutes a structural basis of tissue pathology. From a translational standpoint, elevated LAMA3 expression has been recognized as an independent prognostic indicator in pancreatic ductal adenocarcinoma, whereas LAMA3 promoter methylation is a candidate biomarker for platinum resistance in ovarian cancer. LAMA3-directed gene therapy for JEB has progressed to clinical evaluation. Current limitations in the field are critically examined, and emerging therapeutic approaches, including proteolysis-targeting chimeras (PROTACs), are discussed. Collectively, an integrated framework that connects LAMA3 biology with clinical applications is presented to inform future investigations and precision therapeutic strategies targeting this multifunctional molecule. - Source: PubMed
Publication date: 2026/07/27
Luo ChunmiaoQin FuxingBao MeishuangYao DunweiQin Minzhen - Colorectal cancer (CRC) is one of the global health issues. Current treatments still present major challenges such as off-target cytotoxicity and the emergence of drug resistance, the development of potent and innovative therapeutics is urgently needed. Here, we synthesized copper‑aluminum (CuAl) layered double hydroxides (LDH) using a hydrothermal method and loaded them with the 5-fluorouracil (5-FU) (CuAl-5FU) to improve their anticancer efficacy. The LDHs were 2D-sheeted and rosette-like in shape. The hydrodynamic diameter of CuAl and CuAl-5FU was 568 and 661 nm, respectively. Zeta potential values of CuAl-5FU ranged from +31.39 to +34.93 mV across pH 3 to 9, indicating good colloidal stability. The drug loading and encapsulation efficiency were 18.19% and 36.37%, respectively. Dose-dependent cytotoxicity was seen in HCT-116 and HT-29 CRC cells. Comparatively, CuAl-5FU LDH exhibited greater anticancer activity compared to LDH alone and free 5-FU drug in both monolayer and tumor spheroid models. Mechanistic studies revealed that CuAl-5FU significantly induced reactive oxygen species (ROS) production, mitochondrial membrane depolarization, and promoted apoptosis by upregulating the pro-apoptotic Bax protein and PARP cleavage in both CRC cells. Transcriptomic analysis and qPCR validation revealed the downregulation of oncogenic MAPK signaling and modulation of key genes related to proliferation (JUN, DUSP1, FOSB, EGR1, and FOS), apoptosis (TP53I3, ZMAT3, GADD45A, BBC3, MDM2, TNFRSF10B, E2F1, and ORC1), and cell cycle arrest (CDKN1A and CDC25A). Notably, we identified altered expression of several chemoresistance-related genes (AVPI1, HROB, DDIAS, PTGES, and LAMA3), suggesting the early emergence of adaptive responses in CRC cells. To validate this observation, CuAl-5FU-resistant HCT-116 G3 and HT-29 G2 cell lines were established and their chemoresistant phenotypes were characterized. Indeed, the chemoresistance-associated genes were upregulated, together with significantly higher IC values and clonogenic survival fractions than their respective parental cells. Collectively, these findings suggest that CuAl-5FU improves anticancer activity in CRC cells by modulating multiple genes involved in ROS production, mitochondrial membrane depolarization, apoptosis, and cell cycle regulation. Nevertheless, chemoresistance developed rapidly following repeated treatment, highlighting a potential limitation of this therapeutic approach. Overall, this study provides a new potential strategy for CRC treatment while emphasizing the importance of elucidating the molecular mechanisms underlying acquired chemoresistance. Future studies should also optimize the physicochemical properties of the CuAl-5FU LDH, particularly the large particle size (∼661 nm) by optimizing the hydrothermal synthesis conditions and incorporating surface modifications to further improve the tumor penetration and drug delivery. - Source: PubMed
Publication date: 2026/07/10
Yin YingShi JiayanLu DingyiWang YueranXiang XuemianLiu RuohanHu ZhantuBahadur AliArtoadi Muhammad IdrusZheng ChenxiaoShameli KamyarZhang XiaodongTeow Sin-Yeang