Ask about this productRelated genes to: XIRP2 Blocking Peptide
- Gene:
- XIRP2 NIH gene
- Name:
- xin actin binding repeat containing 2
- Previous symbol:
- CMYA3
- Synonyms:
- -
- Chromosome:
- 2q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-04-03
- Date modifiied:
- 2016-10-05
Related products to: XIRP2 Blocking Peptide
Related articles to: XIRP2 Blocking Peptide
- The Tibetan pig, a highland breed with exceptional adaptability to harsh environments (cold, hypoxia, coarse feed) but poor growth/reproductive traits, was studied to uncover genetic mechanisms and support breeding improvements. - Source: PubMed
Publication date: 2026/02/05
Duan MengqiZhang SongyuanJiao HangShang PengLi ChunliWang Kejun - Cardiac remodeling, including hypertrophy, is associated with alterations in cytosolic Ca homeostasis of cardiac myocytes that spill over into the nucleoplasm. To test whether nuclear Ca signaling acts causally on the development of cardiac hypertrophy, we expressed parvalbumin to buffer nuclear Ca and we blocked nuclear Ca-calmodulin signaling by Adeno-associated virus (AAV)-mediated expression of the calmodulin (CaM) binding-peptide nlsCaMBP4, respectively, in the nuclei of ES cell-derived (Cor.At) and neonatal rat ventricular cardiac myocytes (NRVCM). Expression of nlsCaMBP4, but not parvalbumin, leads to a significant reduction of hypertrophic growth induced by phenylephrine (PE). Expression of nlsCaMBP4 did not alter the amplitude of electrically-evoked intracellular Ca transients in NRVCMs in the absence or presence of PE, and did not affect the PE-evoked increase in store-operated Ca entry. Transcriptome analysis on NRVCMs expressing nlsCaMBP4 revealed that induction of classical hypertrophy markers such as ANF and BNP or MEF2 target genes (such as Srpk3, Xirp1 and Xirp2) were not reduced by nlsCaMBP4 expression. Further analysis of the nuclear Ca-calmodulin-regulated gene pool revealed differential expression of genes involved in mRNA translation, including the translation initiation factor subunits Eif2s1, Eif3d and Eif5, whose upregulation was absent in nlsCaMBP4-treated myocytes. Puromycin assays showed that inhibition of Ca-calmodulin signaling prevented catecholamine-evoked protein translation, suggesting that Ca-calmodulin signaling in the nucleus of cardiac myocytes regulates translation via transcriptional control mechanisms. However, future studies are needed to identify the exact molecular components and machinery that integrate Ca-calmodulin-dependent regulation of transcription, protein translation, and development of cardiac myocyte hypertrophy. - Source: PubMed
Publication date: 2025/12/04
Riedel AnjaMedert RebekkaMonaco SaraGjerga EnioTolksdorf XeniaRichter ChristinMalz MichelleSchrader MeikeKuryshev VladimirBusch MartinJungmann AndreasLöwenthal ZoePhilippaert KoenraadWirth AngelaOttenheijm RogerBenes VladimirMost PatrickDieterich ChristophVölkers MirkoBading HilmarFreichel Marc - Mutations in the desmin gene cause skeletal myopathies and cardiomyopathies. The objective of this study was to elucidate the molecular pathology induced by the expression of R405W mutant desmin in murine skeletal muscle. - Source: PubMed
Batonnet-Pichon SabrinaDelort FlorenceLilienbaum AlainBerwanger CarolinSchultheis DorotheaSchlötzer-Schrehardt UrsulaSchmidt AndreasUebe SteffenBaiche YosraEisenack Tom JTrentini Débora BrochMallek MarkusMill LeonidFerreiro AnaEberhard BettinaLücke ThomasKrüger MarkusThiel ChristianSchröder RolfClemen Christoph S - Postnatal cardiac function in mammals is closely associated with cardiomyocyte proliferation and hypertrophy. However, the molecular mechanisms regulating cardiomyocyte proliferation and hypertrophy have not yet been fully elucidated. Therefore, phenotypic measurements and transcriptomic sequencing were performed on myocardial tissues from 7-day-old (P7) and 3-month-old (3m) female C57BL/6 mice to investigate changes in cardiomyocytes during growth and development and to identify key genes regulating myocardial growth and development. In comparison to 7-day-old mice, 3-month-old mice exhibited a significant increase in heart weight (<0.001) and the cross-sectional area of cardiomyocytes (<0.001). Transcriptome sequencing identified 3,858 differentially expressed genes (DEGs), including 2,021 up-regulated and 1,837 down-regulated genes. Gene Ontology (GO) functional annotation analysis demonstrated that the differentially expressed genes were significantly enriched in biological processes including cell cycle, cell division, cardiac morphogenesis and cellular proliferation. Significantly enriched KEGG pathways were identified, including those for DNA replication, ECM-receptor interaction, the cell cycle, metabolic pathways, and other signaling pathways. Furthermore, key candidate genes associated with myocardial tissue growth and development in mice, including , , , , , , , , and were identified through screening. qRT-PCR validation results demonstrated that the expression trends of the 10 candidate genes related to myocardial growth and development were consistent with the RNA-seq results, confirming the reliability of the sequencing data. The findings of this study provide new insights into the molecular mechanisms underlying the growth and development of mouse myocardial tissue. - Source: PubMed
Zhu Xiao-CongWang Sheng-NanJiang LinLiu Shu-Qin - Head and neck lymphoepithelioma-like carcinoma (HNLEC) is a rare malignancy characterized by distinctive histology and strong association with Epstein-Barr virus infection. However, its genome aberration remains systematically undefined. Through whole-exome sequencing of tumor samples from 20 patients with HNLEC and integrated bioinformatic analyses, this study delineates the somatic mutational landscape of HNLEC for the first time. Through OncodriveCLUST clustering and survival modeling, a set of potentially prognosis-related genes, including EPPK1, EVPL, GLIS1, MUC5B, RP1L1, and XIRP2, were identified. In addition, interrogation of the Drug-Gene Interaction Database highlighted putative therapeutic targets such as CDK13, MUC16, and MUC17. While preliminary, these findings establish the first comprehensive mutational blueprint of HNLEC, providing novel insights into its pathogenesis, potential prognostic determinants, and therapeutic vulnerabilities, and laying a foundation for future translational and clinical research. - Source: PubMed
Publication date: 2025/09/20
Zhang QiangLuo XiaoxiaoFu MinPeng BiZhou YaoLi QianxiaChen XinPeng XiaohongHu YingjiaHu GuangyuanLong Guoxian