AKT1 (myr)
- Known as:
- AKT1 (myr)
- Catalog number:
- 000040A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AKT1 (myr)
Related genes to: AKT1 (myr)
- Gene:
- AKT1 NIH gene
- Name:
- AKT serine/threonine kinase 1
- Previous symbol:
- -
- Synonyms:
- RAC, PKB, PRKBA, AKT
- Chromosome:
- 14q32.33
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
- Gene:
- MYO1B NIH gene
- Name:
- myosin IB
- Previous symbol:
- -
- Synonyms:
- myr1
- Chromosome:
- 2q32.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-04
- Date modifiied:
- 2016-10-05
- Gene:
- MYO1C NIH gene
- Name:
- myosin IC
- Previous symbol:
- -
- Synonyms:
- myr2
- Chromosome:
- 17p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-04
- Date modifiied:
- 2014-11-19
- Gene:
- MYO1D NIH gene
- Name:
- myosin ID
- Previous symbol:
- -
- Synonyms:
- KIAA0727, myr4, PPP1R108
- Chromosome:
- 17q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-04
- Date modifiied:
- 2015-09-04
Related products to: AKT1 (myr)
Related articles to: AKT1 (myr)
- Intracerebral hemorrhage (ICH) is a serious acute cerebrovascular disease with a high death and disability rate. Baicalin plays a neuroprotective role in various diseases, but its regulatory mechanism on ICH remains unclear. In this study, we investigated the protective effects and mechanisms of baicalin in ICH using an ICH mouse model. ICH mouse model was established by injection of collagenase type IV into intracranial in C57BL/6 mice. Neurological function was evaluated by neurological severity scores and the rotarod test. Hemorrhagic foci of brain was evaluated by TTC and hematoxylin-eosin staining. Iron ion deposition in brain was detected by Prussian blue staining. Ferroptosis was evaluated by measuring expression of FTH-1, SLC7A11, GPX4, and TFRC, as well as detecting iron content and levels of glutathione (GSH) and malondialdehyde (MDA). GPX4 expression and apoptosis of brain were detected by immunofluorescence staining and TUNEL assay. Results showed that baicalin improved neurological function and reduced the area of hemorrhagic foci of brain in ICH mouse model. Baicalin decreased iron ion deposition, inhibited ferroptosis and apoptosis, and upregulated GPX4 in brain of ICH mouse model. Moreover, baicalin increased AKT1 phosphorylation and the protein level of Nrf2 in brain of ICH mouse model. Notably, AKT1 inhibitor LY294002 and Nrf2 inhibitor reversed the effects of baicalin on the activation of AKT1/Nrf2/GPX4 axis and the inhibition of ferroptosis in brain of ICH mouse model. Collectively, we demonstrated that baicalin promotes ICH recovery by inhibiting ferroptosis in brain tissue through activation of AKT/Nrf2/GPX4 axis. These results may provide new insights for the study of baicalin in the treatment of ICH. - Source: PubMed
Yu ZhenfeiQian XiaolingWu WeihuaZhang MeiqiLi Ying - To explore the therapeutic mechanism of Flos Sophorae (FS) for treatment of psoriasis. - Source: PubMed
Rao LuDing JiaheWei JiangpingYang YongZhang XiaomeiWang Jirui - To investigate the synergistic mechanism of the traditional Chinese medicine Rosa laevigata Michx. (RLM) for treatment of pulmonary arterial hypertension (PAH). - Source: PubMed
Yang ZiweiLü ChangDong ZhuJi ShuleiBi ShenghuiZhang XuehuaWang Xiaowu - To investigate the effect of Pills (CSP) for alleviating non-alcoholic fatty liver disease (NAFLD) and the underlying mechanism. - Source: PubMed
Luo BiyunYi XinCai YijingZhang ShiqingWang PengLi TongYung Ken Kin LamZhou Pingzheng - J.Ellis is an important medicinal and edible resource. The fruit of J.Ellis contains a natural iridoid called geniposide, which has the ability to dramatically suppress the growth of a number of cancer cell lines. This work examined the impact and potential mechanism of action of geniposide on oral squamous cell carcinoma using network pharmacology, molecular docking, molecular dynamics simulation, and cellular experiments. Based on network pharmacology, 145 potential targets of geniposide in the treatment of OSCC were found. The top five core targets were selected according to the degree values of the nodes, AKT1, EGFR, SRC, HSP90AA1, and PIK3R1, which involved signaling pathways and biological processes, such as the PI3K-Akt signaling pathway, pathways in cancer, phosphorylation, and the regulation of the apoptotic process. Molecular docking showed that geniposide exhibited good binding ability with the core targets AKT1 and EGFR. Molecular dynamics simulations further confirmed the stability of the binding between geniposide and the targets. The results of cell experiments showed that the activity of HSC-3 cells was dose-dependently inhibited by geniposide, and AO/EB staining showed that geniposide was able to induce programmed apoptosis. Meanwhile, it was found that the expressions of p-EGFR, p-AKT, and Bcl-2 were downregulated in HSC-3, and the expressions of PTEN, Bax, and Caspase-3 were upregulated. Geniposide may inhibit OSCC by affecting the PI3K-Akt signaling pathway and apoptotic process by regulating the expressions of p-EGFR, p-AKT, Bcl-2, Bax, Caspase-3, and PTEN. - Source: PubMed
Publication date: 2025/09/22
Wang XueWang JianboHua HuaWei PingChen XuePeng YushengLiu LiYu DongmeiYou XiaozhouYang Siye