CREBL1 antibody - N-terminal region (ARP32167_T100)
- Known as:
- CREBL1 (anti-) - N-terminal region (ARP32167_T100)
- Catalog number:
- arp32167_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CREBL1 antibody - N-terminal region (ARP32167_T100)
Related genes to: CREBL1 antibody - N-terminal region (ARP32167_T100)
- Gene:
- ATF6B NIH gene
- Name:
- activating transcription factor 6 beta
- Previous symbol:
- CREBL1
- Synonyms:
- G13
- Chromosome:
- 6p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-10-09
- Date modifiied:
- 2015-08-28
Related products to: CREBL1 antibody - N-terminal region (ARP32167_T100)
Related articles to: CREBL1 antibody - N-terminal region (ARP32167_T100)
- Rising global temperatures pose a serious threat to wild small mammals' population persistence. In this study, we investigated the molecular mechanisms underlying heat-induced testicular impairment in Brandt's vole (), a dominant small mammal species of the Eurasian temperate steppe. Adult males were subjected to short-term heat exposure at 37 °C, 39 °C, and 41 °C. Heat stress at temperatures ≥ 39 °C significantly reduced the testicular index and caused histopathological damage. Integrated transcriptomic and data-independent acquisition proteomic analyses revealed significant enrichment of pathways related to endoplasmic reticulum protein processing and barrier function. Further molecular validation showed significant upregulation of key ER stress-related markers, including total eIF2α, ATF4, ATF6B, and XBP1, suggesting the potential involvement of the unfolded protein response. Together, these results identify endoplasmic reticulum stress as a key mediator of heat-induced testicular injury and highlight that 41 °C leads to marked activation of ER stress markers and severe testicular impairment in Brandt's voles, even following short-term exposure. - Source: PubMed
Publication date: 2026/09/05
Lou KangJin JiaxueYang YankaiZhao XiaomengZhao LijuanChang ZhiguangLi SenlinWang Zhenlong - : Cabozantinib is a tyrosine kinase inhibitor that primarily targets MET. It has become an important drug in the treatment of renal cell carcinoma (RCC); however, many patients do not respond to cabozantinib treatment and there is no effective next-line therapy. In this study, we identified molecular-targeted drugs that exhibit synergistic effects with cabozantinib using CRISPR/Cas9 screening. : A kinome-wide synthetic lethal CRISPR/Cas9 screen was used to identify target molecules using 786-o RCC cells. A library was generated, and treatment with vehicle or cabozantinib was carried out, followed by next-generation sequencing to identify candidate genes. A combination index based on the Chou-Talalay method was used to evaluate the synergistic effect of cabozantinib through cell viability assays. Xenograft assays were conducted to determine the effect in vivo. : CRISPR/Cas9-based screening revealed four genes (, , , and ) that were candidates for synthetic lethality by cabozantinib in RCC cells. We focused on MEK1 because the MEK1 inhibitor cobimetinib has been approved for melanoma treatment. In a cell proliferation assay using 786-o and A498 RCC cells, the combination of cobimetinib and cabozantinib exhibited a synergistic effect. A xenograft assay also revealed a significant synergistic effect of cobimetinib and cabozantinib. : CRISPR/Cas9 screening identified MEK1 as a candidate for a synthetic lethal target with cabozantinib in RCC. The combined inhibition of MET/VEGFR and MEK1 suppressed compensatory MAPK reactivation and downregulated the PI3K-Akt pathway, including the survival-associated genes PPP2R3B and ATF6B, and produced significant tumor growth suppression in vivo. These findings highlight the potential of cabozantinib plus cobimetinib, an already-FDA-approved MEK inhibitor, as a readily translatable combination strategy to overcome cabozantinib resistance in RCC. - Source: PubMed
Publication date: 2026/07/12
Yoshino HirofumiFukuda IkumiEnokida HidekiSeki NaohikoGoto Yusuke - Maxim (DrT) is a well-known traditional medicinal and edible plant with hepatoprotective effects. In this study, crude polysaccharides of DrT (DrTPs) were obtained using the water extraction-ethanol precipitation method. Autoimmune hepatitis (AIH) models of both mice and ALM12 cells were produced by ConA. The serum liver function indexes (AST and ALT) were examined by ELISA, and liver tissue pathological changes were observed by HE staining. The hepatoprotective mechanism of DrTP80 was explored by RNA sequencing and verified by detecting the protein expressions using Western blot. As a result, DrTP80 could significantly reduce AST and ALT levels in the injured liver and ALM12 cells. DrTP80 also obviously improved the hepatopathological changes in liver tissue induced by ConA. Furthermore, RNA sequencing detected significant differences in gene expression, and the functions of differential genes were focused on TNF and IL-17 signaling pathways. Based on these two signaling pathways, 13 differentially expressed genes (Vcam1, Atf6b, Akt1, Irf1, Map2k3, Lcn2, Hsp90ab1, Anapc5, Traf4, Fosl1, Jun, Cxcl5, Nfκbia) among NC, CRC, and FP groups were screened and verified by Western blot. In conclusion, our results demonstrated that DrTP80 can alleviate immune liver damage induced by ConA, and its hepatoprotective mechanism may be related to regulating TNF and IL-17 signaling pathways. Our findings indicated that DrTP80 could be exploited as a healthy food supplement for the treatment of immune liver injury. - Source: PubMed
Publication date: 2026/03/24
Guo MinWei SaixueCheng BiaobiaoLi Xiaodong - Idiopathic inflammatory myositis (IIM), comprising polymyositis (PM) and dermatomyositis (DM), is a collective term for immune-mediated diseases characterized by skeletal muscle inflammation. Emerging evidence points to an increased incidence of epilepsy in patients with PM/DM. However, the causality and underlying mechanisms behind this association are unclear. Our study aimed to explore the potential causal link between PM/DM and epilepsy, with a focus on immune-mediated mechanisms, using Mendelian randomization (MR) and transcriptome analyses. - Source: PubMed
Liu YingYu YuhangFang ChulongWu QingzhongOu LingliXiao JianhaoDuan KuiJiang TingYe LanHu XiaoFeng Zhanhui - Prostate cancer is one of the most common malignant tumors among men worldwide, and surgery remains its mainstay of treatment. It is unclear how prostate cancer develops and what the most effective drug targets are for treating prostate cancer. Therefore, we sought to identify the genes responsible for prostate cancer. By integrating multidimensional and high-throughput data, proteome wide association studies (PWAS), transcriptome wide association studies (TWAS), single-cell sequencing, functional enrichment, Mendelian randomization (MR), and Bayesian co-localization analyses were used to screen for candidate genes that may contribute to prostate cancer and associate with clinical results of prostate cancer. Our comprehensive analysis showed that protein abundance of eight genes was associated with prostate cancer, four of which were validated at the transcriptome level. These 8 candidate genes (MSMB, PLG, CHMP2B, ATF6B, EGF, TAPBP, GAS1 and MMP7) were validated. After combining single-cell sequencing, Mendelian randomization, and Bayesian co-localization analyses, we identified 1 gene (TAPBP) that is strongly associated with prostate cancer. - Source: PubMed
Publication date: 2025/11/21
Wang XinlongJiang AiminLi ChaoLiu Zhiyong