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
- Metabolic reprogramming is a hallmark of gastric cancer and is essential for sustaining rapid proliferation and malignant progression. The serine synthesis pathway (SSP), a key branch of glycolysis coupled to one-carbon metabolism (OCM), plays a central role in nucleotide biosynthesis, redox homeostasis, and epigenetic regulation. Although aberrant SSP activation has been implicated in gastric cancer, its upstream regulatory mechanisms remain poorly defined. Long non-coding RNAs (lncRNAs) have emerged as critical modulators of oncogenic signaling and metabolism. This study aimed to elucidate the role of the lncRNA SNHG12 in gastric cancer progression and to determine whether it drives metabolic reprogramming through the Wnt/β-catenin-SSP axis. - Source: PubMed
Publication date: 2026/04/30
Zhang NianjieLi TaolangWen Kunming - Metabolic reprogramming has emerged as a key driver of therapy resistance in acute myeloid leukemia (AML). Here, we identify phosphoserine aminotransferase 1 (PSAT1) as a critical metabolic determinant of venetoclax (VEN) resistance through the suppression of ferroptosis. PSAT1 was consistently upregulated in VEN-resistant cell lines and relapsed patient samples. Mechanistically, the transcription factor ATF4 directly bound the PSAT1 promoter, enhancing its expression and subsequently promoting glutathione synthesis, depleting the labile iron pool, and attenuating lipid peroxidation. Concurrently, PSAT1 functioned to restrain JNK/c-Jun signaling. Knockdown of PSAT1 restored VEN sensitivity by triggering ferroptosis and modulating the expression of BCL-2 and GPX4. Clinically, elevated PSAT1 expression predicted poor patient survival. Our findings unveil the ATF4/PSAT1/JNK axis as a master regulator of ferroptosis in AML, revealing a druggable pathway to overcome VEN resistance. - Source: PubMed
Publication date: 2026/04/25
Zhu XunXunHuang WenHuiZhang MingYanTao YanLingZhang Hao - Inborn errors of amino acid metabolism (IEAAM) are genetic defects that lead to the toxic accumulation of metabolites. While the genetic basis of these intoxication-type disorders is well-established, the regulatory role of microRNAs in their pathogenesis remains poorly synthesized. This systematic bioinformatic analysis aims to identify and validate specific miRNA-gene interactions that modulate key metabolic pathways in IEAAM. - Source: PubMed
Publication date: 2026/03/11
Bayrak HarunSharafi ParisaKılıç Mustafa - The N-6-methyladenosine (m6A) modification of mRNA regulates transcript abundance in endocrine therapy (ET)-resistant breast cancer (BCa) cells. We reported that m6A reader HNRNPA2B1 decreased miR-145p and miR-424-5p targeting PSAT1 and miR-34b-5p and miR-876-5p targeting PHGDH, thus stimulating the serine synthesis pathway (SSP) in ET-resistant BCa cells. Here we examined m6A regulation of PSAT1 and PHGDH. We report that siMETTL3 increased miR-145-5p, reducing PSAT1, and miR-34b-5p and miR-876-5p, reducing PHGDH, without affecting HNRNPA2B1 or NFkB and decreasing MYC, known to stimulate PSAT1 and PHGDH transcription. In contrast, the METTL3 inhibitor STM2457 increased METTL3, MYC, HNRNPA2B1, NFkB, PSAT1, PHGDH, and serine synthesis, and decreased the miRNAs. These data suggest that reducing METTL3 protein and inhibition of its catalytic activity have different effects on these targets. Selected results were verified in ET-resistant T47D and ZR-75-1 BCa cells. METTL3's stimulation of translation may play a role in these differences. Indeed, siMETTL3 had no effect on MYC, PHGDH, or PSAT1 pre-mRNA whereas STM2457 increased these pre-mRNAs. Overall, our data support a model for m6A regulation of PHGDH and PSAT1 indirectly through miRNAs that target PHGDH and PSAT1. - Source: PubMed
Publication date: 2026/04/15
Piell Kellianne MVallarta AnnaWilt Ali EAvila-Valdes Bailey LSumlut Mary HGoli NavyaPetri Belinda JHe LiqingZhang XiangClem Brian FKlinge Carolyn M - Clear cell renal cell carcinoma (ccRCC), the most common subtype of kidney cancer, exhibits high molecular heterogeneity and poor clinical prognosis. Current prognostic models often lack functional relevance and fail to reflect the immunometabolic complexity of ccRCC. This study aimed to identify robust, functionally relevant prognostic biomarkers through integrative multi-omics analysis and to develop a clinically applicable risk stratification model. - Source: PubMed
Publication date: 2026/02/27
Du YuelinZheng YanghuangZhang XiaojunWang HongboZhang HelinShang Panfeng