ACTRT1
- Known as:
- ACTRT1
- Catalog number:
- 001110A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACTRT1
Related genes to: ACTRT1
- Gene:
- ACTRT1 NIH gene
- Name:
- actin related protein T1
- Previous symbol:
- -
- Synonyms:
- AIP1, KIAA0705, ARIP1, Arp-T1
- Chromosome:
- Xq25
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-22
- Date modifiied:
- 2016-03-15
Related products to: ACTRT1
Related articles to: ACTRT1
- Actin-related protein T3 (ACTRT3) is localized in the perinuclear theca (PT) of murine spermatids. We generated Actrt3-/- male mice and showed that they are subfertile, with defects of the acrosome first observed during cap phase. Actrt3 deficiency causes reduced protein levels of the trans-Golgi network markers TGN46 and GOPC and mislocalization of the cis-Golgi protein GM130. Reduction of the autophagy markers LC3B, CTSB and mTOR indicates that loss of ACTRT3 leads to impaired Golgi trafficking and autophagic flux, which are required for acrosome biogenesis. In addition, levels of PFN3, a protein involved in acrosome biogenesis, were significantly reduced. Further, co-immunoprecipitation revealed interaction of ACTRT3 with the PT proteins ACTRT1, ACTRT2, ACTL7A, SPEM2 and the sperm surface protein ZPBP. This suggested that ACTRT3 is a part of the complex 3D scaffold of the PT and contributes to ZPBP localization. Mass spectrometry revealed enrichment of cytoskeletal regulators such as CFL1 and CNN1. Expression of Actrt3 caused changes in HEK239T cell shape and F-actin filament distribution, suggesting a role in cytoskeletal shaping. We conclude that lack of ACTRT3 affects acrosome biogenesis, PT structure and actin remodeling. - Source: PubMed
Publication date: 2026/02/11
Kovacevic AndjelaOrdziniak EvaUmer NailaArevalo LenaHinterlang Leo DZiaeipour SanazSuvilla SaraMerges Gina ESchorle Hubert - Male infertility is a common reproductive disorder, affecting about 7% of men in the general population. Despite its prevalence, the cause of infertility is often unknown. This case report presents the results of a comprehensive evaluation of a patient with severe oligoasthenoteratozoospermia and primary infertility. The patient underwent clinical, andrological, and genetic examinations, including semen analysis, transmission electron microscopy, cytogenetic examination, molecular analysis of the AZF locus and the gene, whole-exome sequencing, and Sanger sequencing. Semen analysis revealed severe oligoasthenoteratozoospermia. Transmission electron microscopy showed acrosome detachment from the nucleus in 49% of the spermatozoa. A high percentage (54%) of spermatozoa with insufficiently condensed ("immature") chromatin was also observed. No chromosomal abnormalities, Y chromosome microdeletions, or pathogenic gene variants were identified. Whole-exome sequencing revealed a novel c.821G>C variant (chrX:127185365G>C; NM_138289.4) in the gene (Xq25). This variant was hemizygous in the patient and heterozygous in his mother, as determined by Sanger sequencing. According to the ACMG guidelines (PM2, PP3), this missense variant in the gene was classified as a variant of uncertain clinical significance (VUS). Amino acid conservation and 3D protein modeling predict that the identified variant has a deleterious effect on the protein. This study suggests a potential link between a novel variant and a specific teratozoospermia phenotype. Further functional studies are needed to confirm this association and determine the role of the gene in X-linked male infertility. - Source: PubMed
Publication date: 2025/11/28
Solovova OlgaKhayat SabinaBogolyubov SergeyBragina ElizavetaCherevatova TatianaChernykh Vyacheslav - Tumor progression and therapeutic resistance depend not only on tumor cells but also on the tumor vasculature, a central component of the tumor microenvironment (TME). Accordingly, normalization and remodeling of tumor vessels represent a promising therapeutic strategy, highlighting the urgent need for approaches that selectively and efficiently modulate this compartment. Actrt1 (ArpT1) is an actin-related protein implicated in ciliogenesis, but its roles in the TME are unknown. Here, we show that Actrt1 drives tumor progression through non-hematopoietic cells, with endothelium as a principal site of action. Actrt1 knockout (Actrt1) mice displayed significantly reduced growth of B16F1 and MC38 tumors and improved survival. Bone-marrow chimeras localized this phenotype to the host non-hematopoietic compartment; Actrt1 marrow in WT hosts did not confer protection, whereas WT marrow in Actrt1 hosts did. Immunofluorescence detected Actrt1 in CD31 tumor vessels in vivo. Developmental retinal vascularization was preserved, but endothelial sprouting from Actrt1 aortic rings was reduced, and recovery after hindlimb ischemia was delayed. In Matrigel-tumor plugs, gross vascular ingrowth was decreased. Single-cell RNA-seq of the GFP CD45 stromal fraction resolved 14 clusters; the endothelial fraction was unchanged in proportion, yet Actrt1 deficiency shifted its transcriptome toward immaturity. Histology showed shorter, discontinuous CD31 vessels. Together, our data indicate that Actrt1 promotes tumor growth through non-hematopoietic endothelium by sustaining sprouting and vessel maturation, while developmental angiogenesis remains intact. Targeting Actrt1 may therefore restrain tumor growth by impairing maladaptive angiogenesis and could complement strategies for vascular normalization. - Source: PubMed
Publication date: 2025/11/04
Komuro MarikoMitsui YuichiEdamoto MioWatanabe JunyaNagashima YutoNaito HisamichiIkawa MasahitoSatoh Takashi - - Source: PubMed
Bal ElodiePark Hyun-SookBelaid-Choucair ZakiaKayserili HülyaNaville MagaliMadrange MarineChiticariu ElenaHadj-Rabia SmailCagnard NicolasKuonen FrancoisBachmann DanielHuber MarcelLe Gall CindyCôté FrancineHanein SylvainRosti Rasim ÖzgürAslanger Ayca DilrubaWaisfisz QuintenBodemer ChristineHermine OlivierMorice-Picard FannyLabeille BrunoCaux FrédéricMazereeuw-Hautier JuliettePhilip NicoleLevy NicolasTaieb AlainAvril Marie-FrançoiseHeadon Denis JGyapay GaborMagnaldo ThierryFraitag SylvieCrollius Hugues RoestVabres PierreHohl DanielMunnich ArnoldSmahi Asma - Spermatogenic failure is one of the leading causes of male infertility and its genetic etiology has not yet been fully understood. - Source: PubMed
Publication date: 2024/09/12
Zhou HaiyanYin ZhaochuNi BinLin JiwuLuo ShuweiXie Wanqin