Ask about this productRelated genes to: TIPRL Blocking Peptide
- Gene:
- TIPRL NIH gene
- Name:
- TOR signaling pathway regulator
- Previous symbol:
- -
- Synonyms:
- MGC3794, dJ69E11.3, TIP41, TIPRL1
- Chromosome:
- 1q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-27
- Date modifiied:
- 2016-10-05
Related products to: TIPRL Blocking Peptide
Related articles to: TIPRL Blocking Peptide
- Gain or amplification of chromosome 1q (+1q) is a common genomic alteration occurring in the plasma cells in nearly 40% of multiple myeloma patients. Although it is associated with inferior outcomes and is more common in the relapsed or refractory stages, the impact of +1q at the proteomic level remains unclear. Here, we studied enriched CD138+ plasma cells in newly diagnosed multiple myeloma to uncover molecular alterations associated with +1q. Differential expression analysis revealed significantly increased expression of over 100 proteins encoded by the 1q region, indicating a potential gene dosage effect. Pathway enrichment analysis identified enrichment of cell cycle proteins such as CDK1, MCM complex, CHEK2, PSME3 and NEK7 in cases with +1q gain. Further, protein-protein interaction network analysis showed enrichment of MYC transcriptional targets in +1q cases, including increased expression of TIPRL that is encoded on 1q24. In agreement with these findings, increased TIPRL transcript expression was correlated with +1q across different cytogenetic subgroups in the CoMMpass dataset. Further, high TIPRL expression was associated with poor prognosis in patients from the hyperdiploidy subgroup. Overall, this study highlights the role of proteomics in understanding molecular events associated with chromosomal alterations in MM and identifying potential targets for further functional analysis. - Source: PubMed
Publication date: 2026/04/14
Mangalaparthi Kiran KHsu Joel-SeanWiedmeier-Nutor J ErinSen ParthoStaub JulieBhat Firdous AStein Caleb KAhmann Greg JKumar Shaji KRajkumar S VincentBergsagel P LeifFonseca RafaelBraggio EstebanKandasamy Richard KPandey Akhilesh - One of the reproductive barriers between diverging populations during formation of a new species is the sterility of their hybrids. The driven hybrid male sterility of × hybrids depends on the interaction between PRDM9, a histone methyltransferase that determines the positions of meiotic recombination hotspots, and an as yet unknown X-linked genetic factor within the Hybrid sterility X2 () locus. Here, we report that the microRNA (miRNA) gene cluster is the predicted hybrid sterility factor. We show that removal of the genes restores the fertility of sterile hybrids and improves meiotic synapsis of homologous chromosomes. knockout also restores spermatogenesis in sterile chromosomal translocation carriers, demonstrating that acts as a meiotic checkpoint that can be activated independently of intersubspecific incompatibility. Furthermore, the knockout increases the global recombination rate in hybrids and in parental mice. This demonstrates that is responsible for the phenotypes of the two overlapping genetic loci, the engaged in fertility of hybrids and the Meiotic recombination 1 () controlling the recombination rate. The finding of enlarged clusters in all European samples tested and the identification of differentially expressed targets suggest that the reproductive barrier between the two subspecies is sensitive to copy number variation of genes. Together, the underdominant interaction between and provides a rare example of Dobzhansky-Muller incompatibility in hybrids of closely related species, making it accessible for further analysis at the molecular level. - Source: PubMed
Publication date: 2025/10/02
Jansa PetrTanieli GiordanoVucinic KimLustyk DianaFusek KarelValiskova BarboraMorimoto KentoMizuno SeiyaUllrich KristianOdenthal-Hesse LindaProvaznik JanBenes VladimirPfeiferova LucieKolar MichalGergelits VáclavPialek JaroslavForejt Jiri - The TOR signaling pathway regulator-like (TIPRL) gene plays a multifaceted role in cancer, yet its pan-cancer profile remains underexplored. This study investigates TIPRL expression across multiple cancers and its associations with survival, genetic alterations, immune infiltration, and functional pathways, providing insights into TIPRL's role as a potential prognostic and therapeutic target. - Source: PubMed
Publication date: 2025/03/15
Zhang XuezhongXue HaoLv YuanyuanZhou YuntaoSha KaihuiLiu Tonggang - In the 55th round of CAPRI, we used enhanced AlphaFold2 (AF2) sampling and data-driven docking. Our AF2 protocol relies on Wallner's massive sampling approach, which combines different AF2 versions and sampling parameters to produce thousands of models per target. For T231 (an antibody-peptide complex) and T232 (PP2A:TIPRL complex), we employed a 50-fold reduced MinnieFold sampling and a custom ranking approach, leading to a top-ranking medium prediction in both cases. For T233 and T234 (two antibody bound MHC I complexes), we followed data-driven docking, which did not lead to an acceptable model. Our post-CAPRI55 analysis showed that if we had used our MinnieFold approach on T233 and T234, we could have submitted a medium-quality model for T233 as well. In the scoring challenge, we utilized the scoring function of FoldX, which was effective in selecting acceptable models for T231 and medium-quality models for T232. Our success, especially in predicting and ranking a medium-quality model for T231 and potentially for T233, underscores the feasibility of green and accurate enhanced AF2 sampling in antibody complex prediction. - Source: PubMed
Publication date: 2025/03/03
Savaş BüşraYılmazbilek İremÖzsan AtakanKaraca Ezgi - Frequent recurrence and metastasis caused by cancer stem cells (CSCs) are major challenges in lung cancer treatment. Therefore, identifying and characterizing specific CSC targets are crucial for the success of prospective targeted therapies. In this study, it is found that upregulated TOR Signaling Pathway Regulator-Like (TIPRL) in lung CSCs causes sustained activation of the calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2) signaling pathway by binding to CaMKK2, thereby maintaining stemness and survival. CaMKK2-mediated activation of CaM kinase 4 (CaMK4) leads to phosphorylation of cAMP response element-binding protein (CREB) at Ser129 and Ser133, which is necessary for its maximum activation and the downstream constitutive expression of its target genes (Bcl2 and HMG20A). TIPRL depletion sensitizes lung CSCs to afatinib-induced cell death and reduces distal metastasis of lung cancer in vivo. It is determined that CREB activates the transcription of TIPRL in lung CSCs. The positive feedback loop consisting of CREB and TIPRL induces the sustained activation of the CaMKK2-CaMK4-CREB axis as a driving force and upregulates the expression of stemness- and survival-related genes, promoting tumorigenesis in patients with lung cancer. Thus, TIPRL and the CaMKK2 signaling axis may be promising targets for overcoming drug resistance and reducing metastasis in lung cancer. - Source: PubMed
Publication date: 2024/07/30
Song In-SungJeong Yu-JeongYun Jae KwangLee JiminYang Hae-JunPark Young-HoKim Sun-UkHong Seung-MoLee Peter C WLee Geun DongJang Sung-Wuk