PRKAR1B 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- PRKAR1B 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00005575-T02
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- PRKAR1B 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: PRKAR1B 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- PRKAR1B NIH gene
- Name:
- protein kinase cAMP-dependent type I regulatory subunit beta
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-17
- Date modifiied:
- 2016-01-27
Related products to: PRKAR1B 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: PRKAR1B 293T Cell Transient Overexpression Lysate(Denatured)
- The metabolic mechanisms by which aging blunts CD8 T cell antitumor and pathogen defense remain unknown. We demonstrate that the aged microenvironment induces CD8 T cell exhaustion by reducing β-hydroxybutyrate (3HB) bioavailability. Aging represses hepatic BDH1-dependent 3HB synthesis, restricting SLC16A1-mediated 3HB uptake. Hepatic BDH1 ablation recapitulates age-associated CD8 T cell dysfunction, compromising antiviral and antitumor immunity, whereas 3HB supplementation reverses these deficits via protein β-hydroxybutyrylation. Using a 3HB-derived chemical probe, 3Halk, together with functional screening, we identify PRKAR1B as a primary effector of 3HB signaling. PRKAR1B β-hydroxybutyrylation inhibits the transcription factor cyclic AMP (cAMP)-responsive element modulator (CREM), which activates T cell exhaustion-related gene expression. Age-associated 3HB depletion enhances CREM-dependent transcription, sustaining CD8 T cell exhaustion. Consistently, the aged microenvironment compromises chimeric antigen receptor (CAR) T antitumor activity, which is substantially restored by 3HB treatment. Collectively, this study uncovers a hepatic metabolism-derived 3HB-CREM axis governing CD8 T cell immunosenescence, highlighting 3HB as a viable immunorestorative strategy to improve immunotherapy outcomes in aged individuals. - Source: PubMed
Publication date: 2026/09/03
Xiao YifengZhang YanlingZhao ZihaoZhang ZijianZhang XiaohuiChen PengjuGu JinZhu HaichuanJiang PengCheng Jie - Head and neck squamous cell carcinoma (HNSC) is one of the most prevalent malignancies worldwide. PRKAR1B, a regulatory component of protein kinase A (PKA), has been widely investigated for its potential involvement in tumorigenesis across different diseases. However, its specific role in HNSC remains elusive. In this study, significant differences in PRKAR1B expression were observed across various cancer types. PRKAR1B was highly expressed in HNSC and was strongly associated with poor prognosis in HNSC patients. Moreover, it was identified as an independent prognostic factor significantly associated with clinical parameters. Correlation analysis revealed that PRKAR1B expression was associated with genes such as C7orf50, EIF3B, TBRG4, DDX56, and BRAT1. Additionally, it was associated with TMB and was correlated with the infiltration of immune cells such as M1 macrophages, activated mast cells, and eosinophils. Notably, PRKAR1B was identified as a predictive marker for the efficacy of CTLA-4 inhibitors, with high PRKAR1B expression potentially conferring superior therapeutic responses. Drug sensitivity analysis further suggested that Lapatinib and Erlotinib may be beneficial in HNSC patients with high PRKAR1B expression. Meanwhile, experiments showed that PRKAR1B knockdown inhibited HNSC cell proliferation and migration. Lastly, PRKAR1B protein expression was upregulated in clinical HNSC samples. Overall, this study thoroughly examined PRKAR1B expression and its prognostic significance in HNSC, investigated related molecular pathways and immune cell interactions, and validated its role via experiments. - Source: PubMed
Publication date: 2026/02/20
Zhao PengLi KangXiu WuFengLiu ZhaokunHuang YanxiaoJiang YoufangZhang PengPeng Lixiang - Proteins can be denatured and precipitated under different denaturation conditions, and ligand bound proteins are more resistant to denaturing induced precipitation. Consequently, ligand target proteins can be identified by measuring solubility shifts. Nowadays, numerous methods have been developed to screen ligand target proteins based on different denaturation mechanisms. However, due to the different responses of proteins to different denaturation conditions, there is a significant complementary between these methods. Direct pooling of the denatured supernatants from different denaturation strategies can utilize this complementary, however, the pooling procedure inevitably averages the ligand-induced solubility shift across conditions, significantly compromising target identification sensitivity. - Source: PubMed
Publication date: 2025/09/29
Ma YanniZhang XiaoleiShi LongrunYan JiayangWang KeyunYe Mingliang - Marbach-Schaaf neurodevelopmental syndrome (MASNS) is an ultra-rare, monogenic disease caused by pathogenic variation in PRKAR1B, which codes for the R1β regulatory subunit of protein kinase A (PKA), a key effector of cAMP signaling within the nervous system. This work provides a comprehensive clinical description of 12 subjects with pathogenic PRKAR1B variants, including two individuals with a heterozygous deletion including PRKAR1B, supporting haploinsufficiency as a possible mechanism of disease. Phenotypic information was obtained by interview, using a systematic multi-dimensional questionnaire. Besides expanding the evidence for established MASNS phenotypes like developmental delay, ID, ASD, pain insensitivity, as well as mild dysmorphisms, we broaden the clinical spectrum through the description of new and underreported findings, in particular increased body weight. In addition, the presence of genomic deletions suggests dosage sensitivity of PRKAR1B, demonstrating that both sequence and copy number variants should be considered in diagnostic testing. This work gives valuable insight into the pathophysiology of MASNS and sets a framework upon which to design future mechanistic studies of PKA signaling in brain development. - Source: PubMed
Publication date: 2025/10/29
Burkart SebastianGuzeloglu TarikSoares Ana RValenzuela IreneTizzano Eduardo FGómez-Andres DavidPasquier LaurentLegendre MarineBerges CamilleThevenon JulienGauthier MarjolaineHeid CalebRanum EllyShen JosephFrees MichelleSchmidtke Michael WPilar CaroSchaaf Christian P - Many transcript isoforms generated by intronic polyadenylation (IPA) encode isoforms of canonical proteins. Microproteins are an emerging class of small proteins translated from small open reading frames (sORFs) in noncoding RNAs and mRNAs, but their production by IPA isoforms is unknown. - Source: PubMed
Publication date: 2025/10/23
Devaux AlexandreTanaka IrisFouilleul QuentinHeneman-Masurel AmélieCadix MandyMichallet SophieChakraborty AlinaLabbé Céline MFontrodona NicolasSahoo SubhadarsiniClaude Jean-BaptisteDeloger MarcGestraud PierreTessier LudovicMortada HusseinLameiras SoniaRaynal VirginieBaulande SylvainServant NicolasAuboeuf DidierEymin BéatriceVagner StéphanDutertre Martin