Ask about this productRelated genes to: CTDSP1 antibody
- Gene:
- CTDSP1 NIH gene
- Name:
- CTD small phosphatase 1
- Previous symbol:
- -
- Synonyms:
- NLIIF, SCP1
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-27
- Date modifiied:
- 2015-11-06
Related products to: CTDSP1 antibody
Related articles to: CTDSP1 antibody
- Integrated preclinical systematic review and meta-analysis with basic experimental research. - Source: PubMed
Publication date: 2026/06/05
Shang ZhizhongWang Xin - Spermatogonial stem cells (SSCs) are unipotent germline cells with emerging pluripotent potential under specific in vitro conditions. Understanding their capacity for reprogramming and the molecular mechanisms involved offers valuable insights into regenerative medicine and fertility preservation. SSCs were isolated from Oct4-GFP C57BL/6 transgenic mice using enzymatic digestion and cultured in defined media. Under these conditions, ES-like colonies emerged expressing pluripotency markers. These cells were characterized by immunocytochemistry, teratoma assays, and transcriptomic analyses using bulk and single-cell RNA sequencing datasets. Gene expression profiles were compared with ESCs and SSCs using datasets from GEO (GSE43850, GSE38776, GSE149512). Protein-protein interaction (PPI) networks and co-expression modules were explored through STRING, Cytoscape, and WGCNA. ES-like cells derived from SSCs exhibited strong expression of OCT4, DAZL, and VASA. Transcriptomic analysis revealed key differentially expressed genes and shared regulatory networks with ESCs. WGCNA identified key co-expression modules and hub regulatory RNA binding genes (Ctdsp1, Rest, and Stra8) potentially responsible for the reprogramming process. Teratoma assays confirmed pluripotency, and single-cell RNA-seq validated expression of critical markers in cultured SSCs. This study demonstrates that SSCs can acquire pluripotency features and be reprogrammed into ES-like cells. The integration of transcriptomic and network-based analyses reveals novel insights into the molecular drivers of SSC reprogramming, highlighting their potential utility in stem cell-based therapies and male fertility preservation. - Source: PubMed
Publication date: 2025/10/20
Shakeri Abroudi AliAzizi HosseinKhalid Abdullah HewaAlsaffar Marwa FadhilSkutella Thomas - Amino acids and ammonia serve as sources of nitrogen for cell growth and were previously thought to have similar effects on yeast. Consistent with this idea, depletion of either of these two nitrogen sources inhibits the target of rapamycin complex 1 (TORC1), leading to induction of macroautophagy/autophagy and inhibition of cell growth. In this study, we show that Whi2 and the haloacid dehalogenase (HAD)-type phosphatases Psr1 and Psr2 distinguish between these two nitrogen sources in , as the Whi2-Psr1-Psr2 complex inhibits TORC1 in response to low leucine but not in the absence of nitrogen. In contrast, a parallel pathway controlled by Npr2 and Npr3, components of the Seh1-associated complex inhibiting TORC1 (SEACIT), suppress TORC1 under both low leucine- and nitrogen-depletion conditions. Co-immunoprecipitations with mutants of Whi2, Psr1, Psr2 and fragments of Tor1 support the model that Whi2 recruits Psr1 and Psr2 to TORC1. In accordance, the interaction between Whi2 and Tor1 appears to increase under low leucine but decreases under nitrogen-depletion conditions. Although the targets of Psr1 and Psr2 phosphatases are not known, mutation of their active sites abolishes their inhibitory effects on TORC1. Consistent with the conservation of HAD phosphatases across species, human HAD phosphatases CTDSP1 (CTD small phosphatase 1), CTDSP2, and CTDSPL can functionally replace Psr1 and Psr2 in yeast, restoring TORC1 inhibition and autophagy activation in response to low leucine conditions. - Source: PubMed
Publication date: 2025/03/27
Wang YitaoPing YangZhou RuiWang GuiqinZhang YuYang XueyuZhao MingjunLiu DongshengKulkarni MadhuraLamb HeatherNiu QingweiHardwick J MarieTeng Xinchen - Porocarcinoma is a malignant sweat gland tumour differentiated toward the upper part of the sweat duct and may arise from the transformation of a preexisting benign poroma. In 2019, Sekine et al. demonstrated the presence of YAP1::MAML2 and YAP1::NUTM1 fusions in most poromas and porocarcinomas. Recently, our group identified PAK2-fusions in a subset of benign poromas. Herein we report a series of 12 porocarcinoma cases harbouring PAK1/2/3 fusions. - Source: PubMed
Publication date: 2024/05/24
Kervarrec ThibaultWestphal DannaPissaloux DanielLegrand MélanieTirode FranckNeuhart AnneDrouot FrancoiseBecker Jürgen CMacagno NicolasSeris AliceJouary ThomasBeltzung FannyJullie Marie-LaureHarms Paul WCribier BernardMourah SamiaJouenne FanélieFromont GaelleLouveau BaptisteMancini MaxenceKazakov Dmitry Vde la Fouchardière ArnaudBattistella Maxime - Clear cell renal cell carcinoma (ccRCC) accounts for 80-90% of kidney cancers worldwide. Small C-terminal domain phosphatases CTDSP1, CTDSP2, and CTDSPL (also known as SCP1, 2, 3) are involved in the regulation of several important pathways associated with carcinogenesis. In various cancer types, these phosphatases may demonstrate either antitumor or oncogenic activity. Tumor-suppressive activity of these phosphatases in kidney cancer has been shown previously, but in general case, the antitumor activity may be dependent on the choice of cell line. In the present work, transfection of the Caki-1 cell line (ccRCC morphologic phenotype) with expression constructs containing the coding regions of these genes resulted in inhibition of cell growth in vitro in the case of ( < 0.001) and ( < 0.05) but not . The analysis of The Cancer Genome Atlas (TCGA) data showed differential expression of some of genes and of their target, . These results were confirmed by quantitative RT-PCR using an independent sample of primary ccRCC tumors ( = 52). We observed downregulation and found a positive correlation of expression for two gene pairs: and ( = 0.76; < 0.001) and and ( = 0.38; < 0.05). Survival analysis based on TCGA data demonstrated a strong association of lower expression of , , , and with poor survival of ccRCC patients ( < 0.001). In addition, according to TCGA, , , and were differently expressed in two subtypes of ccRCC-ccA and ccB, characterized by different survival rates. These results confirm that and have tumor suppressor properties in ccRCC and reflect their association with the more aggressive ccRCC phenotype. - Source: PubMed
Publication date: 2023/08/19
Krasnov George SPuzanov Grigory ADashinimaev Erdem BVishnyakova Khava SKondratieva Tatiana TChegodaev Yegor SPostnov Anton YSenchenko Vera NYegorov Yegor E