Temporal Lobe Lysate
- Known as:
- Temporal Lobe Lysate
- Catalog number:
- 21-176
- Product Quantity:
- 0.2 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- Temporal Lobe Lysate
Related genes to: Temporal Lobe Lysate
- Gene:
- AKT1S1 NIH gene
- Name:
- AKT1 substrate 1
- Previous symbol:
- -
- Synonyms:
- PRAS40, MGC2865, Lobe
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-04
- Date modifiied:
- 2016-04-26
Related products to: Temporal Lobe Lysate
Related articles to: Temporal Lobe Lysate
- The anterior pituitary integrates endocrine regulation, cellular growth, and adaptive responses. Adipokines, secreted mainly by adipose tissue, act as hormonal signals linking metabolism, inflammation, appetite, and reproduction. They regulate hypothalamic-pituitary-ovarian axis by modulating hormone secretion and intracellular signaling. The presence of adipokine receptors in anterior pituitary suggests local metabolic-endocrine interactions. Omentin-1, predominantly expressed in visceral adipose tissue, participates in glucose metabolism and ovarian steroid regulation. Recent findings indicate that omentin-1 modulates tropic hormones, their receptors, and adipokine balance in anterior pituitary cells. We hypothesized that omentin-1 affects protein expression and signaling pathways involved in pituitary cell proliferation and apoptosis. This study examined its effects in anterior pituitary cells from Large White and Meishan pigs. Proteomic analysis identified 230 candidate differentially abundant proteins after omentin-1 treatment: 30 downregulated and 3 upregulated in Large White pigs, and 107 downregulated and 90 upregulated in Meishan pigs, associated with enriched 116 Gene Ontology terms. Key proteins were associated with cell cycle, DNA replication, gene expression, and posttranscriptional/posttranslational regulation. Responses differed between breeds. CDK5RAP2 and SIX1 were linked to proliferative control in Large White pigs, whereas AKT1S1 and RHOA were among the proteins associated with the broader proteomic response observed in Meishan pigs. Meishan pigs showed dynamic apoptotic protein regulation, including HTRA2, PARP2, and DFFA. Complementary in vitro experiments demonstrated that omentin-1 downregulated cyclins and caspase-3, upregulated BCL2, increased BCL2/BAX ratio, and modulated ERK1/2, AKT, AMPKα, and STAT3 phosphorylation. Together, these findings suggest that omentin-1 modulates proteomic networks and intracellular signaling associated with anterior pituitary cell function during the mid-luteal phase of the estrous cycle. - Source: PubMed
Publication date: 2026/08/19
Respekta-Długosz NataliaKubicka KarolinaGreggio AleksandraŚwiderska BiankaMalinowska AgataRytelewska EdytaOpydo MałgorzataDupont JoëlleKamiński TadeuszSmolińska NinaRak Agnieszka - As a traditional element of Chinese medicine, is well known for promoting adolescent growth, yet its active fractions and underlying molecular mechanisms remain unclear. In this study, the aqueous extract of was subjected to in vitro simulated gastrointestinal digestion and ultrafiltration to separate three molecular weight fractions (<10 kDa, 10-30 kDa, >30 kDa). Their chemical profiles were characterized, and osteogenic activities were systematically evaluated using cell assays, a juvenile rat model, and integrated transcriptomics and data-independent acquisition (DIA) proteomics. Results revealed that chemical profiling showed the >30 kDa fraction was mainly composed of hemocyanin subunits, and the 10-30 kDa fraction was enriched in growth-related amino acids and steroid derivatives; functionally, the 10-30 kDa fraction promoted preosteoblast proliferation and early differentiation via enhanced alkaline phosphatase (ALP) activity, while the >30 kDa fraction dominated late osteoblast maturation and mineralization. Both fractions significantly increased rat body and bone length by expanding growth plate proliferative zones and elevating serum insulin-like growth factor-1 (IGF-1)/bone morphogenetic protein-2 (BMP-2) levels. Transcriptomic and proteomic analyses identified vascular endothelial growth factor (VEGF), Wingless-related integration site (Wnt), phosphatidylinositol 3-kinase-protein kinase B (PI3K-Akt), and extracellular matrix (ECM)-receptor interaction as potential core regulatory pathways. Integrated multi-omics analysis further confirmed Frizzled-related protein B () and AKT1 substrate 1 () as candidate key regulatory targets enriched in the Wnt and adenosine monophosphate-activated protein kinase (AMPK) signaling pathways. These findings elucidate the multi-fraction, multi-pathway mechanism of in promoting skeletal development, providing scientific evidence for its traditional use and a theoretical basis for growth-promoting functional food development. - Source: PubMed
Publication date: 2026/06/30
Huang LianghuaPan ZhaojiBai MengGuo JiyanXiao JianGao Chenghai - Serine/threonine-proline (S/T-P) phosphorylation is a fundamental mechanism maintaining cellular homeostasis. Although glycogen synthase kinase 3β (GSK3β) is a key regulator in ischemic stroke, the contribution of its proline-directed kinase activity to cellular dysfunction and disease progression remains unclear. Here, we developed Nb.29E9, a nanobody that selectively targets the proline-directed kinase domain of GSK3β. Under ischemic conditions, Nb.29E9 inhibited S/T-P phosphorylation of key substrates, including RNA-binding motif protein 38 (RBM38), HIF1α, and p53, thereby enhancing neuronal and microglial viability while reducing oxidative stress and neuroinflammation. Phosphoproteomic analysis revealed broad reprogramming of S/T-P phosphorylation networks. In mice after ischemic injury, Nb.29E9 delivered via a brain-penetrant, MMP-9-responsive nanoparticle reduced infarct volume, restored neurovascular integrity, and improved motor function. Mechanistically, Nb.29E9 corrected pathological hyperphosphorylation of SMAD2/3-Thr8 (TGFβ signaling), calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2)-Ser495 (AMPK pathway), and AKT1 substrate 1 (AKT1S1)-Ser183 (mTORC1 regulation). These findings demonstrate that GSK3β's intrinsic proline-directed kinase activity drives ischemic neurodegeneration, establishing its pathogenic role in vivo. - Source: PubMed
Publication date: 2026/06/09
Li LanLi MuyangSun LeiYang YingWu YuanshunYin ZiyiWang AnniZhou PeiyangLuo ShaoxiangChen JianQin JunAi ZhibingYuan ZilongDong ZhiqiangZhang Min - BACKGROUND: Pressure overload first leads to compensated hypertrophy and secondary to heart failure. m6A-RNA methylation is a fast process for the adaptation of cell composition. m6A-RNA-methylation is regulated by the demethylase, fat mass and obesity-associated protein (FTO), and FTO protein levels are diminished in heart failure. Cardiomyocyte-specific FTO-transgenic/knockout-mice have shown the relevance of FTO in pressure overload remodeling. However, its functional downstream regulatory mechanisms are still unclear. In this study, we discover the harmful signaling pathways that are triggered by m6A imbalance and FTO loss, which eventually lead to adverse cardiac remodeling and heart failure. METHODS: FTOcKO animals were generated by crossing FTOfl/fl mice with α-MHC Cre mice using Cre-lox system. Control and the FTOcKO animals groups were subjected to TAC (transverse aortic constriction) surgery. Echocardiography was performed 1-week post-TAC surgery. MeRIP (m6A RNA immunoprecipitation) sequencing was performed from the heart tissues of mice after one week TAC surgery. Additionally, the mechanistical interrelation between the signaling pathways during FTO loss and adverse cardiac remodeling were investigated in human iPS-CMs (hiPS-CMs). RESULTS: One week post-TAC surgery, FTOcKO mice showed impaired cardiac function (EF: CreC TAC (45%) vs. FTOcKO TAC (25%), p < 0.0001) and increased LVID (CreC TAC(3.9 mm) vs. FTOcKO TAC (4.8 mm), p < 0.0001), indicating a lack of adaption to pressure overload. Knockdown of FTO in hiPS-cardiomyocytes also reduced endothelin-induced hypertrophic response. MeRIP-seq data of FTOcKO mice showed that the differentially hypermethylated transcripts were associated with cardiac apoptosis inhibition (CDK1, CFLAR), mTORC1 signaling pathway (AKT1S1) and autophagy regulation (TFEB). mTORC1 was identified as a central player of dysregulation with hyperactivation of its canonical substrates phospho-S6K1 (Thr 389) and phospho-S6 (ser235/236) ex-vivo (FTOcKO) and in-vitro (FTO-KD-hiPS-CMs). Moreover, FTO-deficient cardiomyocytes cause autophagic flux impairment and defective autophagy. The effect of atrophy and induced apoptosis upon FTO-m6A imbalance could be rescued by pharmacological inhibiton of the mTORC1-S6K1 pathway. CONCLUSIONS: Downregulation of FTO leads to mTORC1-S6K1 hyperactivation that shift the compensative hypertrophic response to atrophy and apoptosis leading to progressive heart failure. These findings might pave the way for the development of novel therapeutic targets for the early phases of heart failure treatments. - Source: PubMed
Publication date: 2025/12/02
Annamalai KarthikaDilliker SoniyaBuchholz EricCastro-Hernández RicardoPanyam NikitaPommeranz AlessaWiederhake PascalWery von Limont NellyHempel NinaEbner VerenaSwarnkar SurabhiMohamed Belal AStreckfuss-Bömeke KatrinSteffens SabineHerzig StephanEbert AntjeFischer AndreToischer Karl - Immune checkpoint blockade (ICB) has revolutionized the treatment landscape of non-small cell lung cancer (NSCLC), yet primary resistance remains a significant clinical challenge. Recent evidence implicates PRAS40 (AKT1S1) in regulating cellular survival and immune responses, but its role in immunotherapy resistance is not fully understood. - Source: PubMed
Publication date: 2025/10/10
Mao NingHe CuiKuang JiaWang ChunguangYang Zhao