Ask about this productRelated genes to: PSAT1 antibody
- Gene:
- PSAT1 NIH gene
- Name:
- phosphoserine aminotransferase 1
- Previous symbol:
- -
- Synonyms:
- PSA
- Chromosome:
- 9q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-19
- Date modifiied:
- 2014-11-19
Related products to: PSAT1 antibody
Related articles to: PSAT1 antibody
- While CAR-T cell therapy has transformed outcomes in B-cell malignancies, most genomic insights originate from clinical trials. There is a paucity of data describing molecular changes during CAR-T manufacturing in real-world practice, particularly for non-US CAR constructs. - Source: PubMed
Publication date: 2026/09/03
Das NupurMehta PrashantGupta KusumKatharia RahulPabbi SwatiMishra PravasMorya Soni - Thyroid cancer is the most common type of endocrine malignancy, and its aggressive types are diagnosed at advanced stage due to limited treatment options. This study aimed to identify upregulated SLC7A5 across thyroid cancer cell types using an integrated transcriptomics approach. Total RNA was extracted from different samples. Differential expression analysis was performed through DESeq2. Functional enrichment analyses were performed to explore key pathways. The PPI network was built using the STRING database to investigate the functional relationships among significantly differentially expressed genes. Differential expression analysis revealed that SLC7A5 was significantly upregulated in KTC-1. GO and KEGG analyses were enriched with cell adhesion, protein binding, extracellular exosome, RNA processing, ECM-receptor interactions, and focal adhesion. The PPI network analysis showed the interaction of SLC7A5 with TERF1, CARD10, PSAT1, SIRPA, and MYC. Western blot analysis revealed that expression of mTOR was not elevated in KTC-1. Overall, these results could provide valuable insights for further validation in thyroid cancer therapy. - Source: PubMed
Publication date: 2026/09/03
Naeem MuhammadWu NanWu YangNawaz ShahidJing RenLuo YuanbinYi Shijian - Aposematism and crypsis are contrasting antipredator strategies widespread across animal taxa, yet their genetic basis remains poorly understood in amphibians. Aposematic species advertise toxicity through conspicuous coloration, whereas cryptic species rely on concealment to avoid predators. The granular poison frog, Oophaga granulifera, with allopatric aposematic (red) and cryptic (green) morphs, provides an excellent system to explore the molecular mechanisms underlying transitions between these strategies. We used a comparative genomic approach, mapping RNA-seq reads to the Oophaga sylvatica reference genome and a de novo assembled O. granulifera superTranscriptome, to characterize its population genetics and detect genes with single nucleotide polymorphisms under positive selection. We identified two main genetic clusters with strong divergence between green and red populations. We found 283 SNPs showing signatures compatible with positive selection using the reference genome and 749 SNPs using the reference superTranscriptome, indicating greater sensitivity of the latter approach in capturing species-specific genetic variation. Some of these SNPs occur in coloration-related genes, including genes involved in melanin synthesis (DVL2, FZD7, GNAI1), pteridine synthesis (MYCBP2), iridophore development (IMPDH1, PSAT1), carotenoid metabolism (BCO1, RARG, RETSAT), and pigmentation variation. Our findings highlight the complex genetic basis of color diversity in anurans and the value of generating species-specific genomic resources for non-model organism's research. - Source: PubMed
Publication date: 2026/08/25
Cajigas Gandia AnaisaPröhl HeikeMetzger JuliaRodrÃguez Ariel - Lung cancer bone metastasis carries a poor prognosis, yet the metabolic determinants driving tumour-stroma crosstalk remain largely elusive. Despite extensive investigations into itaconate, a prominent immunometabolite implicated in macrophage polarization, the precise mechanisms by which it modulates bone metastasis remain unresolved. Integrating metabolomics and transcriptomics profiling, the molecular landscape of lung cancer bone metastasis is delineated and the mechanistic role of itaconate is uncovered. Further ubiquitination proteomics of tumour cells and CRISPR-Cas9-mediated knockout of the gene encoding immune-responsive gene 1 (IRG1) confirmed the results in an animal model of lung cancer bone metastasis. The macrophage-to-myofibroblast transition generated cancer-associated fibroblasts that secreted elevated levels of itaconate, significantly accelerating tumour growth. A drug affinity responsive target stability screening pinpointed heat shock protein family A member 8 (HSPA8) as a direct molecular target of itaconate. Mechanistically, itaconate promoted HSPA8 ubiquitination and subsequent proteasomal degradation, thereby releasing activated transcription factor 4 (ATF4) from cytosolic sequestration. Liberated ATF4 translocated to the nucleus, where it bound the promoter region of phosphoserine aminotransferase 1 (PSAT1) to upregulate its expression. In vivo validation demonstrated that administration of adeno-associated virus-delivered PSAT1 short hairpin RNA or of a cell-penetrating itaconate antagonist significantly reduced tumour burden and prolonged survival. Our findings elucidate an unappreciated metabolic reprogramming axis in lung cancer bone metastases: macrophage-to-myofibroblast transition-derived itaconate alleviated cytoplasmic sequestration of ATF4 via HSPA8 ubiquitination, thereby activating its transcriptional target PSAT1. This mechanism converts immunometabolic byproducts into pro-tumorigenic signals that enhance bone metastasis. Notably, the HSPA8-ATF4-PSAT1 axis was identified as a key regulatory pathway governing metabolic reprogramming, thereby establishing a translational framework for targeting immunometabolic crosstalk in bone metastasis therapy. - Source: PubMed
Publication date: 2026/08/05
Qian JinTan ZhidanWang JinfengWei TiantianHuang ChongquanCheng ShiZhong GuoqingZou HuizhenKang XiaSun LinchongZhang Yu - The progression and immune escape of HCC are closely regulated by endoplasmic reticulum stress (ERS). However, the associated ceRNA regulatory networks and their prognostic value remain to be systematically elucidated. Here, we sought to establish a prognostic signature derived from an ERS-associated ceRNA network and to investigate its relationship with the tumor immune microenvironment. We integrated TCGA-LIHC transcriptomic data with the MSigDB ERS gene set to identify ERS-associated differentially expressed genes and construct a ceRNA regulatory network. Using a forward search strategy with 10-fold cross-validation, we screened candidate genes to select the optimal prognostic combination and constructed a multigene Cox regression signature. External validation was performed in the independent microarray cohort GSE14520. By integrating single-cell transcriptomics, CIBERSORT, ESTIMATE, TIDE, and drug sensitivity analyses, we revealed immune microenvironment characteristics associated with this signature. Based on the ceRNA network's eight core ERS mRNAs, an optimal three-gene signature comprising , , and was selected via forward search. The signature demonstrated robust prognostic discrimination in the TCGA training cohort (C-index = 0.653) and was independently corroborated in the external GSE14520 dataset (C-index = 0.584, log-rank = 0.008). The signature was confirmed as an independent prognostic indicator by multivariable Cox regression. Functional enrichment analysis demonstrated a marked accumulation of cell-cycle-related pathways in the high-risk group, notably DNA replication and the spindle assembly checkpoint. Single-cell transcriptomic profiling showed that and were predominantly expressed by tumor epithelial cells, whereas and were mainly detected in macrophages and fibroblasts. Drug sensitivity analysis indicated that the high-risk group was more sensitive to drugs such as docetaxel and AZD5582, consistent with the upregulation of proliferation pathways in this group; in the low-risk group, VE-822 exhibited selective sensitivity. This study established a three-gene prognostic signature based on the ERS-associated ceRNA network. The signature demonstrated robust prognostic stratification capabilities in cross-platform validation and revealed molecular characteristics centered on uncontrolled cell-cycle progression, as well as an immunosuppressive microenvironment, in the high-risk group, providing an exploratory tool for prognostic assessment and treatment strategy selection in hepatocellular carcinoma (HCC). - Source: PubMed
Publication date: 2026/07/21
Shi QingpingGao ShuangChen BeiyanShen MingliHan Jieru