Polyclonal Rabbit RALBP1 Antibody
- Known as:
- Polyclonal Rabbit RALBP1 Antibody
- Catalog number:
- abx000767
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Polyclonal Rabbit RALBP1 Antibody
Related genes to: Polyclonal Rabbit RALBP1 Antibody
- Gene:
- RALBP1 NIH gene
- Name:
- ralA binding protein 1
- Previous symbol:
- -
- Synonyms:
- RLIP76, RIP1, RIP
- Chromosome:
- 18p11.22
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-11
- Date modifiied:
- 2014-11-19
Related products to: Polyclonal Rabbit RALBP1 Antibody
Related articles to: Polyclonal Rabbit RALBP1 Antibody
- Apigenin, a naturally occurring flavonoid with low toxicity, exhibits anticancer activity, yet its effects on microRNAs (miRNAs) and downstream gene networks in esophageal squamous cell carcinoma (ESCC) remain unclear. Here, we evaluated apigenin's antitumor effects in TE-1 and Eca-109 cells, assessing proliferation, apoptosis, colony formation, and invasion. Differentially expressed miRNAs were identified via small RNA sequencing, and candidate target genes were predicted, annotated using GO and KEGG analyses, and validated by qRT-PCR, revealing miRNA-mediated regulatory mechanisms underlying apigenin's inhibitory effects in ESCC. Apigenin markedly suppressed cell proliferation, clonogenic growth, wound closure, and invasive capacity, while promoting apoptosis in a dose-dependent manner. In TE-1 cells, apigenin upregulated hsa-let-7c-3p, hsa-miR-374c-3p, hsa-miR-3177-3p hsa-miR-4454, and hsa-miR-4728-3p, while downregulating hsa-miR-573, hsa-miR-548az-5p, hsa-miR-33b-5p, hsa-miR-4479, and hsa-miR-3198. Correspondingly, tumor-associated target genes including , , , and were upregulated, whereas , , , and were suppressed. In Eca-109 cells, apigenin altered the expression of distinct miRNAs, including the upregulation of hsa-miR-891-5p, hsa-miR-3170, hsa-miR-4421, and hsa-miR-675-5p and the downregulation of hsa-miR-153, hsa-miR-3188, and hsa-miR-4435, thereby modulating key oncogenic targets such as , , and . Functional enrichment analyses indicated that apigenin-regulated genes are involved in multiple cancer-related pathways across cytoplasmic and nuclear compartments. Overall, these results suggest that apigenin suppresses ESCC progression via coordinated miRNA-mRNA regulation, highlighting its potential as a therapeutic agent. - Source: PubMed
Publication date: 2026/02/28
Amjad NoumanMajid MuhammadSun ZhaojianBasnet RajeshRasool KashafWu LinpingLi Zhiyuan - The overexpression and/or mutations of Epidermal Growth Factor Receptor (EGFR) are associated with the progression of several cancers. Thiourea derivatives have emerged as promising compounds to target EGFR for cancer treatment. - Source: PubMed
Publication date: 2026/03/06
Abu-Zaid RaniaAbusara Osama HHussein ButhainaSaqallah Fadi GAlbujuq Nader R - Cerebral microhemorrhages (CMHs) contribute to cognitive decline and motor deficits. Inhibiting A1 astrocyte polarization can attenuate brain injury and promote recovery after experimental intracerebral hemorrhage. Despite RIP1 is a known mediator of neurological impairment in hemorrhage models, it is not known whether it regulates astrocytic phenotypic switching to influence CMH progression. Here, a mouse model of hypertension-induced CMHs was established by co-administration of Ang II and L-NAME. Following hypertension induction, daily neurological assessments showed progressively declining scores, indicating ongoing CMH development. RIP1 silencing delayed CMH onset, reduced cumulative incidence, and alleviated hypertension-induced deficits including gait abnormalities, impaired spatial learning and memory, blood-brain barrier (BBB) dysfunction, and A1 astrocyte polarization. In vitro, primary mouse astrocytes were exposed to hemoglobin to simulate the microhemorrhagic microenvironment. RIP1 silencing attenuated hemoglobin-induced A1 polarization and promoted a shift toward the A2 phenotype. Furthermore, RIP1 knockdown counteracted the detrimental effects of A1-polarized astrocytes on endothelial function, as evidenced by improved endothelial cell proliferation, migration, and tube formation. Mechanistically, RIP1 knockdown facilitated the transition from A1 to A2 astrocytic phenotype by activating autophagy and suppressing the NF-κB-NLRP3 inflammasome pathway, thereby mitigating hypertension-induced BBB disruption following CMHs. In conclusion, RIP1 silencing alleviates BBB disruption following hypertension-induced CMHs by promoting autophagy-mediated A2 astrocyte polarization. - Source: PubMed
Publication date: 2026/03/12
Hu GengyaoShi RuiLi YangWang LuojunZhao JingjingLiu LijuanWei DongZhang Xiao - Perioperative neurocognitive disorders (PND) is the most prevalent central nervous system (CNS) complication in older patients after surgery. Clinical and animal studies have shown that anesthesia/surgery can cause increased glycolysis and lactate production in the CNS, which is closely related to PND. However, the specific molecular mechanism by which lactate affect cognitive function remains unclear. Recent research has demonstrated that lactate can lead to neurodegenerative diseases by regulating target gene transcription through histone lactylation. The involvement of histone lactylation in PND remains to be fully elucidated. Here, we found that anesthesia/surgery induced synaptic plasticity and cognitive deficits in aged mice, accompanied by elevated hippocampal lactate and histone H3 lysine 9 lactylation (H3K9la) in neurons. Inhibiting lactate production with 2-deoxyglucose can effectively reduce synaptic and cognitive damage. To elucidate the involvement and mechanism of H3K9la in PND, we screened the target gene regulated by H3K9la through CUT&Tag sequencing. The upregulation of RalBP1 can phosphorylate Drp1 Ser616 and promote mitochondrial fission, which leads to synaptic impairment of hippocampal neurons. Knockdown of inhibits hippocampal neurons excessive mitochondria fission and synaptic impairment of aged mice after anesthesia/surgery, and therefore alleviates cognitive deficits. Thus, the H3K9la-RalBP1-Drp1 Ser616 pathways may provide a prospective intervention target for PND. - Source: PubMed
Publication date: 2026/02/13
Meng FanbingCao SiluWu WeifengZhang MeixianJing QiXie ZhengSun XiaoxiaoSong JianFei MiaomiaoChen QianGao XiaofeiLi Cheng - Key findings of this study with potential clinical relevance include:• RLIP is an attractive therapeutic target with the ability to suppress human OC at multiple stages of development.• Reducing RLIP levels significantly inhibits OC cell growth and enhances apoptosis compared with controls.• RLIP blockade/depletion may serve as a broad-spectrum therapeutic strategy that remains effective regardless of common pathway differences among OC subtypes.• This is the first evidence from integrated in vitro and in vivo studies demonstrating the strong therapeutic promise of RLIP-targeting agents for treating metastatic OC. - Source: PubMed
Publication date: 2026/01/30
Krishna B MadhuGarg PankajHorne DavidKulkarni PrakashSalgia RaviSinghal Sharad S