TORC2 Blocking Peptide
- Known as:
- TORC2 Blocking Peptide
- Catalog number:
- 33r-11024
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- TORC2 Blocking Peptide
Related genes to: TORC2 Blocking Peptide
- Gene:
- CRTC2 NIH gene
- Name:
- CREB regulated transcription coactivator 2
- Previous symbol:
- -
- Synonyms:
- TORC2
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-24
- Date modifiied:
- 2014-11-19
Related products to: TORC2 Blocking Peptide
Related articles to: TORC2 Blocking Peptide
- Disruption in alveolar type 2 epithelial cells (AT2s) homeostasis by oxidative stress plays an essential role in the pathogenesis of acute lung injury (ALI). However, significant discrepancies remain in understanding the mechanisms for AT2 as a main target for reactive oxygen species (ROS). Herein, we show that STUB1, an E3 ligase involved in protein homeostasis, was dominantly expressed in AT2s. Mild levels of ROS potentiated Nrf2-mediated transactivation of the STUB1 gene via activation of the ERK signaling, whereas high levels of ROS compromised STUB1 expression by dampening STUB1 protein half-life. Ablation of Stub1 in AT2s caused failure in conferring K63-mediated nonproteolytic polyubiquitination of SIK3 (salt-inducible kinase 3), which in turn abrogated CRTC2 (CREB-regulated transcription co-activator 2) substrate binding for SIK3 and thereby triggered CREB signaling-mediated proinflammatory phenotypes. Consequently, disruption in STUB1/SIK3 signaling aggravated lung edema, augmented inflammatory infiltrate, and increased AT2 apoptosis in vivo. Mice lacking STUB1 also demonstrated increased susceptibility to ischemia-reperfusion and overventilation-induced lung injury. These findings unambiguously uncover STUB1 as a critical post-translational regulator of ALI severity and outcomes. - Source: PubMed
Publication date: 2026/05/04
Tian FengXie NianlinZhong DaixingNi YunfengZhang BinghuaLiang XiaohuaMa JunGong XiaokangSun ZhuochenZhao JieJiang TaoLi Wei - Non-small cell lung cancer (NSCLC) patients with tumors harboring mutations are resistant to standard of care anti-PD-1/PD-L1 blockade. For this patient population there are no currently available tailored treatments, underlying the critical need to discover effective therapeutic strategies. In this study, we dissected the molecular mechanisms responsible for -mediated resistance to immune checkpoint blockade (ICB) and identified CRTC2, a coactivator of the transcription factor cAMP response element-binding protein (CREB), as a key signaling node regulating -dependent cell-extrinsic functions. CRTC2 deletion remodeled the immune profiles of -KO tumors and resensitized them to anti-PD-1 treatment, comparably to -proficient tumors. Mechanistically, the abrogation of the binding between CRTC2 and CREB was sufficient to restore sensitivity to immunotherapy. These findings provide critical insights into the central role of CRTC2 in modulating response to ICB and identify the disruption of CRTC2-CREB interaction as a potential therapeutic approach for this patient population. - Source: PubMed
Publication date: 2026/04/22
Robay DimitriAckermann OleLaborde LaurentShi XingyiOreglia FedericoStump RamonaCiaghi SabinaGalli Giorgio GHolzer LauraVillemin LorraineWagner JoelWu JinchengLee Lang HoBossen ClaudiaMourikis Thanos PGabriel MillicentRuddy DavidYu HaiyanJohannessen CoryFerretti StephaneCosta Carlotta - Understanding the genetic basis of growth and fat deposition is crucial for improving beef productivity in Kalmyk cattle, a breed well adapted to the extreme climatic conditions of Kazakhstan. The present study aimed to determine the effects of single-nucleotide polymorphisms (SNPs) in the CRTC2 and ELOVL6 genes on intramuscular fat content and to evaluate their associations with growth and meat quality traits in 18-month-old Kalmyk heifers raised under different environmental conditions. - Source: PubMed
Publication date: 2025/12/19
Kazhgaliyev NurlybayNurgulsim KasterGabbassov MirasMakhanbetova AizhanZhanabayev AssylbekTerlikbayev AscarAssanbayev TolegenToishimanov MaxatSharapatov Tlekbol - Circadian disruption contributes to hepatocellular carcinoma (HCC) progression. This study aimed to develop a CT-based radiomics model to non-invasively predict circadian rhythm (CR) gene expression profiles for improved prognostic assessment. - Source: PubMed
Publication date: 2025/12/25
Zhao JiaxinZhou HuiyingWang ChengZhang WenluoPang YujiangZheng HuilinZhang LeiZhou JieHu Zhenhua - Acute myeloid leukemia (AML) is a hematologic malignancy characterized by the malignant proliferation of myeloid progenitor cells. Although the introduction of the B-cell lymphoma-2 (BCL-2) inhibitor Venetoclax (VEN) has significantly improved patient outcomes and established it as a first-line treatment, high rates of drug resistance and relapse remain major clinical challenges. We integrated RUNX3 chromatin immunoprecipitation sequencing (ChIP-seq) data with the GAPIA2 database to identify CRTC2 as a key candidate gene. Subsequently, we employed qRT-PCR to compare CRTC2 expression levels between donors and AML patients. The role of CRTC2 in apoptosis was further validated through knockdown and overexpression experiments in various cell lines. To investigate the impact of CRTC2 on AML progression, we established a cell line-derived xenograft (CDX) model. The proportion of human CD45-positive (hCD45) cells in the bone marrow and liver was assessed, and histological examination was conducted using HE staining, along with peripheral blood smear analysis. In addressing VEN resistance, we analyzed CRTC2 expression patterns in clinical samples and explored the synergistic therapeutic effect of a CRTC2 inhibitor in combination with VEN. To further elucidate the underlying molecular mechanisms, we performed mitochondrial function assays and analyzed mitochondrial translation-related proteins. Clinical analyses have demonstrated that elevated expression levels of CRTC2, a downstream target of RUNX3, are significantly correlated with poor prognosis in patients with AML. Functional experiments have shown that CRTC2 plays a role in disease progression by modulating apoptosis in AML cells. The knockdown of CRTC2 was observed to delay disease progression in CDX mouse models. Additional investigations revealed a positive correlation between CRTC2 expression and resistance to VEN in AML cells, with CRTC2 inhibition synergistically enhancing VEN's cytotoxic effects. Mechanistic studies suggest that increased mitochondrial activity contributes to VEN resistance, thereby identifying a potential molecular target for overcoming drug resistance. CRTC2 is a key regulator in AML, with high expression levels promoting disease progression and resistance to VEN. Inhibiting CRTC2 reduces mitochondrial translation and energy reserves, increasing AML cell sensitivity to VEN. These results highlight CRTC2 as a promising therapeutic target and suggest a new strategy to overcome VEN resistance. - Source: PubMed
Liang XiaomeiZheng YiluJiang BangxueHuang YulingTang JingDeng HaimeiZhang ChenxingZhao MinyiLin Dongjun