IgG,Akt2 (Ab_474)
- Known as:
- Immunoglobulin G,Akt2 (Ab_474)
- Catalog number:
- 210014
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- IgG Akt2 (Ab_474)
Related genes to: IgG,Akt2 (Ab_474)
- Gene:
- AKT2 NIH gene
- Name:
- AKT serine/threonine kinase 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-05
- Date modifiied:
- 2016-10-05
Related products to: IgG,Akt2 (Ab_474)
Alkaline Phosphatase Conjugated Affinity Purified anti-Swine IgG (H&L) [Goat] Secondary_Antibodies Alkaline Phosphatase Conjugated Affinity Purified anti_Swine IgG (H&L) [Goat](20S)_3alpha_amino_5alpha_pregnan_20_ (20S)_3alpha_amino_5al(3β,24S)-Cholest-5-ene-3,24-diol CAS: 474-73-7 Formula: C27H46O2(5-Lactoglobulin IgG ELISA, Allergies(Arg8)-Vasopressin - Purified Antiserum - IgG(Arg8)-Vasopressin - Purified Antiserum - IgG, Host Rabbit(Arg8)-Vasopressin - Purified Antiserum - IgG, Host Rabbit(Arg8)-Vasopressin - Purified Antiserum - IgG, Host: Rabbit(Arg8)-Vasopressin - Purified Antiserum - IgG, Host: Rabbit(Arg8)_Vasopressin _ Purified Antiserum _ IgG, Host Rabbit(Arg8)_Vasopressin _ Purified Antiserum _ IgG, Host Rabbit(Arg8)_Vasopressin _ Purified Antiserum _ IgG, Host Rabbit(Arg8)_Vasopressin _ Purified Antiserum _ IgG, Host Rabbit(D-Ser(tBu)6,Azagly10)-LHRH (Goserelin) - Purified Antiserum - IgG Related articles to: IgG,Akt2 (Ab_474)
- Triple-negative breast cancer (TNBC) is characterized by hypoxia and impaired fidelity to DNA repair and the activation of survival pathways. However, the role of specific AKT isoforms, particularly AKT2, in regulating residual homologous recombination (HR) activity and PARP inhibitor sensitivity under hypoxic stress remains unclear. This study aimed to establish the effect of AKT2 on hypoxia-induced defects in HR repair, DNA damage accretion, and therapeutic outcomes of PARP inhibition in TNBC. TNBC cells were cultured under chronic hypoxia (1% O) or normoxia. Western blotting was used to measure protein expression and activation of HR- and hypoxia-related markers, including, pAKT (Ser473), RAD51, BRCA1, γH2AX, HIF-1α, and CHK1/CHK2. Immunofluorescence was used to assess the presence of RAD51 foci following 4 Gy of irradiation as a functional measure of HR activity. A cell viability assay was used to determine the sensitivity to olaparib. In vitro findings were confirmed in orthotopic xenograft models with stable AKT2 knockdown. Hypoxia in tumors was measured through pimonidazole staining and HIF-1α expression. Hypoxia increases HIF-1α expression and activates AKT signaling. In our model, chronic hypoxia suppressed RAD51, p-BRCA1, and checkpoint signaling, whereas total BRCA1 did not change and RAD51 foci decreased, indicating impaired and context-dependent disruption of HR. Only AKT2 silencing reduced RAD51 and p-BRCA1 under hypoxia, indicating an isoform-specific role for AKT2 in HR maintenance. In AKT2-deficient hypoxic cells, there was accumulation of persistent γH2AX and a corresponding repair defect. Functionally, AKT2 loss significantly enhanced olaparib sensitivity, resulting in marked RAD51 loss, robust γH2AX accumulation, and decreased viability. Knockdown of AKT2 in vivo increased the efficacy of olaparib, decreasing tumor weight and hypoxia and increasing the extent of DNA damage and suppression of HR markers, demonstrating a synergistic disruption of hypoxia-driven survival pathways. AKT2 plays a vital role in the regulation of the HR repair and hypoxia-driven survival in TNBC. Although hypoxia impaired HR through suppression of RAD51, p-BRCA1, and checkpoint signaling, AKT2 preserved residual HR activity required for tumor cell survival under hypoxic stress. Its loss disrupts HR components, enhances sustained DNA damage, inhibits tumor hypoxia and sensitizes hypoxic tumors dramatically to PARP inhibition. These findings support a mechanistic model in which AKT2 enables hypoxic TNBC cells to tolerate HR dysfunction and survive genotoxic stress, thereby contributing to therapeutic resistance. These results establish AKT2 as a therapeutic target to counteract resistance in hypoxia and increase the efficacy of PARP inhibitors in TNBC. Although AKT2-selective inhibitors have been reported, they remain largely preclinical. Accordingly, our findings support AKT2 as a promising therapeutic target and warrant further validation using AKT2-selective pharmacologic inhibition. - Source: PubMed
Liang YingKong DeyuZhang YiZhao ZhijingLv LiYin ZheAhmad AjazJiang Zongye - Macrophage polarization into M1 (pro-inflammatory) or M2 (anti-inflammatory) phenotypes is essential for immune responses and tissue homeostasis. While transcriptional and post-transcriptional mechanisms controlling this process have been characterized, the contribution of alternative mRNA polyadenylation (APA) to polarization requires clarification. Using human monocytic cell lines, we demonstrate that CFIm25, a key APA regulator, controls macrophage polarization states. CFIm25 overexpression enhances M1 characteristics, including nitric oxide production, CD80 expression, pro-inflammatory cytokine secretion, phagocytosis, migration, and cancer cell killing, while suppressing M2 traits. CFIm25 knockdown produces opposite effects. Mechanistically, CFIm25 promotes the proximal polyadenylation of AKT2 mRNA, generating shorter transcripts with enhanced stability and translational efficiency that increase Akt2 protein levels and amplify NF-κB signaling. Blocking the proximal site with antisense oligonucleotides reduces Akt2 expression and induces M2-like phenotypes. These findings establish APA as a critical regulator of macrophage polarization and identify the CFIm25-Akt2-NF-κB axis as a potential therapeutic target for modulating immune responses. - Source: PubMed
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Mukherjee SrimoyeeBarua AtishNaseri MarziehMoore Claire L - Acute lung injury (ALI) is a severe, life-threatening inflammatory condition, characterized by uncontrolled neutrophilic inflammation and tissue damage. That emphasized the urgent need for innovative pharmacologic therapies. The aim of this study was to investigate the effects of Celastrol, a major bioactive compound extracted from the Thunder of God Vine, and the underlying mechanisms of its impact on ALI. - Source: PubMed
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Zhang YuYang YunLin ZhifengChen RikenQiang XinhuaLi ChangGuo WeiguangCao JunYe YinongZhou Lixin - Early recurrence after curative resection remains a major challenge in hepatocellular carcinoma (HCC), particularly in hepatitis B virus (HBV)-related cases. Liquid biopsy using circulating microRNAs (miRNAs) offers a non-invasive approach to identify molecular markers predictive of recurrence. - Source: PubMed
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