BASP1
- Known as:
- BASP1
- Catalog number:
- 002416A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- BASP1
Related genes to: BASP1
- Gene:
- BASP1 NIH gene
- Name:
- brain abundant membrane attached signal protein 1
- Previous symbol:
- -
- Synonyms:
- NAP-22, NAP22, CAP23, CAP-23
- Chromosome:
- 5p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-08
- Date modifiied:
- 2016-01-06
Related products to: BASP1
Related articles to: BASP1
- Mechanisms by which primary tumor cells acquire metastatic capability through metabolic and signaling adaptations are currently poorly understood. We demonstrate that tumor-intrinsic ceramide metabolism, amplified by dietary fat, initiates colorectal cancer metastasis. We observed that dietary fat exposure triggers a sustained increase in de novo ceramide biosynthesis, mediated by the dihydroceramide desaturase . Ceramide accumulation activates yes-associated protein (YAP) through protein phosphatase 2A (PP2A)-mediated dephosphorylation, promoting a durable shift toward a distinct YAP-driven regenerative (YAP-DR) program, marked by , that promotes metastasis. Selective elimination of cancer cells prevented metastatic seeding. loss reduced ceramide levels, YAP activity, YAP-DR signatures, and metastasis without affecting primary tumor growth, whereas blocking ceramide degradation enhanced YAP activity and metastasis. These findings identify ceramide-induced YAP signaling as a key mediator of metastatic initiation, operating independently of primary tumor expansion. - Source: PubMed
Publication date: 2026/09/24
Goswami SwagataZhang QimingYildiz Abdullah BurakDas Adhikari UpasanaRaghawan Akhouri KishoreBulliard ManonSedhain SabhyataDarawshi OdaiCelik Cigdem ElifCansiz FeyzaKrempe Constantin PRösler JonasAllies GabrieleMeckelmann Sven WChi ChiashinHormann Felix-LevinHeiles SvenSedlak JosephGrace WesleyEng GeorgeReich EthanAlquati ChiaraWilliams Kevin JRead Benjamin JRashan Edrees HLi ZhixinJnawali AnupOrtiz Jose AJain ChestaWhittaker Charles AYilmaz Osman HDeshpande VikramSchmitz Oliver JSickmann AlbertYork Autumn GKwon Douglas SNeumann UlfFedorova MariaVander Heiden Matthew GOgretmen BesimSethi Nilay STasdogan AlpaslanYilmaz Ömer H - Plasma biomarkers, particularly brain-derived phosphorylated-tau (BD-p-tau) species, hold promise as screening tools for Alzheimer's disease (AD). However, their ability to reflect AD pathology remains understudied in community settings. In a community-based sample, we examined associations between plasma biomarkers and cerebral amyloid (Aβ) deposition, and whether kidney function modified these associations. - Source: PubMed
Publication date: 2026/07/31
Akinci MugeAziz FrooghGuzman DianaCheung LinaKong Jian XSilver StephanieEimicke JosephSimoes SabrinaTeresi Jeanne ABrickman Adam MLao PatrickLuchsinger José A - The retinal pigment epithelium (RPE) contributes to retinal homeostasis in part through non-coding RNA (ncRNA) regulatory networks, and its degeneration underlies blinding diseases. How physical and paracrine regenerative stimuli affect the RPE non-coding transcriptome remains unknown. We performed RNA-seq on ARPE-19 cells in a full-factorial design of four treatments (CTRL, QMR, a patient blood-derived secretome, and QMR+SECRETOME) two oxidative-stress states (basal and tert-butyl hydroperoxide [tBHP]-induced), and three time points (8, 24, 72 h). lncRNAs and circRNAs were sub-classified and mapped via GO enrichment and in silico ceRNA prediction. PCA identified QMR as the dominant driver of transcriptomic variance, priming ARPE-19 cells to integrate paracrine signals. Analysis across six factorial contrasts identified 105 modulated non-coding transcripts, including a pan-responsive antisense core (, ) and condition-specific shifts in master lincRNAs (, ). QMR+SECRETOME produced a distinct combinatorial transcriptomic signature. was exclusively upregulated by QMR, while was preferentially hyperactivated by combinatorial treatment. ceRNA analysis predicted potential sponging of miR-29, miR-21, and miR-155, which may derepress BMP signaling and extracellular matrix remodeling. QMR reshapes the ARPE-19 non-coding transcriptome and enables a non-additive transcriptomic response to secretome co-treatment. The QMR-secretome-circRNA axis identifies candidate non-coding biomarkers and therapeutic targets for retinal regeneration. - Source: PubMed
Publication date: 2026/07/22
Alibrandi SimonaMordà DomenicoScimone ConcettaD'Ascola AngelaAliquò FedericaAbate GiorgiaPozzato GianantonioScalinci Sergio ZaccariaD'Angelo RosaliaSidoti AntoninaDonato Luigi - The persistent HIV reservoir constitutes the main obstacle to curing HIV/AIDS disease. Our understanding of how non-productive HIV infections are established in primary human CD4 T cells during the first round of infection is still incomplete. In this study, we leverage the HIV reporter virus pMorpheus-V5 to delineate cellular expression patterns upregulated in non-productively infected stem cell memory (T) CD4 T cells. We find that CD4 T harboring non-productive proviruses display a distinct transcriptomic signature comprising 118 upregulated genes, distinct from that of productively infected cells as well as from negative-exposed and mock-infected cells. Among the cellular genes most upregulated in CD4 T cells harboring non-productive proviruses are CCR4-binding migratory chemokines (CCL22, CCL17), tryptophan catabolic enzymes (IDO1, KYNU), and genes encoding cytoskeletal rearrangement proteins (BASP1, TNFAIP2). Flow cytometry-based analyses confirm that non-productively infected CD4 T cells are enriched for CCL22 and IDO1 co-expression compared to other CD4 T memory subsets, underscoring a CD4 T cell subset specificity for the upregulation of these two immune gene sets associated with non-productive infections. These findings suggest that primary human CD4 T harboring non-productive proviruses display a distinct immunoregulatory phenotype which may facilitate immune evasion and contribute to the persistence of the HIV reservoir. - Source: PubMed
Publication date: 2026/06/25
Butta Giacomo MAlburquerque BremyKearns CharlotteHadas YoavVanDyck Max WScaglioni SusannaPeña NoahWong Hoi TongLevendosky ElizabethGleason CharlesLin XiaoManganaro LaraPinto DalilaMulder Lubbertus C FSimon Viviana - Myeloid-derived suppressor cells (MDSCs) are essential immunosuppressive elements found within the tumor microenvironment (TME) and significantly influence the development of breast cancer (BC). Given their critical role in cancer progression, identifying MDSC-related genes is urgently needed to develop more effective treatment strategies for BC patients. The integration of bulk RNA-seq data from the TCGA-BC cohort alongside scRNA-seq data from the GSE176078 dataset was performed for identifying MDSC-related genes through bioinformatic analysis. Subsequently, the potential of the hub gene BASP1 in predicting prognosis and immune infiltration in BC was evaluated. Furthermore, the functional role of BASP1 in BC was investigated both in vitro and in vivo. Notably, BASP1 levels were significantly higher in BC tissues than in adjacent normal tissues, and elevated BASP1 expression was closely associated with adverse clinical outcomes. Additionally, BC patients with increased BASP1 levels exhibited increased infiltration of immunosuppressive cells (M2 macrophages and Tregs) but reduced infiltration of CD8 + T cells. Functionally, downregulation of BASP1 was observed to suppress BC cell proliferation and migration in vitro through inactivation of AKT and ERK signalings. Mechanistically, BASP1 in 4T1 cells promoted MDSC migration, at least partially, via upregulating CXCL12 secretion, while BASP1 in MDSCs directly suppressed T cell function. In vivo experiments showed that BASP1 knockdown markedly inhibited tumor growth in mouse models bearing 4T1 tumors, accompanied by decreased MDSCs infiltration and increased Granzyme B + CD8 + T cell accumulation in tumor tissues. Collectively, BASP1 may serve as a potential prognostic biomarker and a therapeutic target for BC intervention, functioning both as a pro-tumorigenic gene and as an immunomodulatory molecule that shapes an immunosuppressive microenvironment. - Source: PubMed
Publication date: 2026/06/23
Hu HaijieFeng XiaominYan Zhi'anQi FuzhongLi DonghaiLuo Xuegang