# MROH9 ## Overview MROH9, or Maestro Heat-Like Repeat Family Member 9, is a gene located in the human genome that encodes the protein maestro heat like repeat family member 9. This protein, although not extensively characterized, is implicated in various biological processes and medical conditions based on genetic association studies. The precise function of the MROH9 protein remains largely unknown, with existing literature primarily focusing on its role in relation to specific diseases rather than its fundamental biological functions. Research has linked MROH9 to conditions such as hypercalciuria, pancreatic adenocarcinoma, and osteosarcoma, suggesting its involvement in pathological processes including cancer development and progression (Guleray2024Decreased; Xu2018Genetic; Wu2022Novel). Further studies are required to elucidate the specific molecular and cellular functions of MROH9 and its encoded protein, which could potentially reveal novel therapeutic targets or biomarkers for these diseases. ## Function The specific molecular functions and roles of the MROH9 protein in healthy human cells are not well characterized in the available literature. The gene MROH9, known as Maestro Heat-Like Repeat Family Member 9, is mentioned in various studies, but detailed descriptions of its molecular activities, cellular roles, or organismal outcomes are largely unexplored or not explicitly detailed. For instance, while MROH9 is identified in the context of genetic studies related to conditions like hypercalciuria and pancreatic adenocarcinoma, these references primarily discuss its presence and expression rather than its functional roles in cellular or physiological processes (Guleray2024Decreased; Wu2022Novel). Moreover, in studies where MROH9 is mentioned, such as those involving chromosomal deletions or genome-wide analyses, the focus remains on its association with certain conditions or its differential expression rather than on elucidating its specific functions within the cell (Choquet2020A; Ashraf2015Two). Therefore, the precise molecular functions, cellular roles, and physiological implications of the MROH9 protein in healthy human cells remain to be fully determined and require further investigation. ## Clinical Significance MROH9 has been implicated in various medical conditions through genetic studies, although its direct causative role in specific diseases remains to be fully established. Research has shown potential associations between mutations or expression levels of MROH9 and several types of cancer. For instance, MROH9 mutations have been identified in osteosarcoma patients, suggesting a possible role in the genetic landscape of this cancer, particularly concerning tumor heterogeneity and metastatic behavior (Xu2018Genetic). Additionally, MROH9 is highly expressed in a high-risk group of pancreatic adenocarcinoma (PAAD), indicating its potential involvement in the oncology process for these patients (Wu2022Novel). This gene has also been identified as a significant necroptosis-related gene, serving as an independent prognostic marker in PAAD, further underscoring its relevance in cancer prognosis (Wu2022Novel). Outside of cancer, MROH9 has been noted in the context of chromosomal deletions associated with developmental and skeletal abnormalities, such as those observed in patients with the 1q24 deletion syndrome. However, the specific impact of MROH9 deletion on the clinical phenotype of these patients has not been detailed (Ashraf2015Two). Overall, while MROH9 is associated with several pathological conditions, further research is necessary to clarify its exact role and mechanisms in these diseases. ## References [1. (Guleray2024Decreased) Naz Guleray Lafci, Mark van Goor, Semra Cetinkaya, Jenny van der Wijst, Melisa Acun, Fatma Kurt Colak, Arda Cetinkaya, and Joost Hoenderop. Decreased calcium permeability caused by biallelic trpv5 mutation leads to autosomal recessive renal calcium-wasting hypercalciuria. European Journal of Human Genetics, March 2024. URL: http://dx.doi.org/10.1038/s41431-024-01589-9, doi:10.1038/s41431-024-01589-9. (1 citations) 10.1038/s41431-024-01589-9](https://doi.org/10.1038/s41431-024-01589-9) [2. (Choquet2020A) Hélène Choquet, Ronald B. Melles, Jie Yin, Thomas J. Hoffmann, Khanh K. Thai, Mark N. Kvale, Yambazi Banda, Alison J. Hardcastle, Stephen J. Tuft, M. Maria Glymour, Catherine Schaefer, Neil Risch, K. Saidas Nair, Pirro G. Hysi, and Eric Jorgenson. A multiethnic genome-wide analysis of 44,039 individuals identifies 41 new loci associated with central corneal thickness. Communications Biology, June 2020. URL: http://dx.doi.org/10.1038/s42003-020-1037-7, doi:10.1038/s42003-020-1037-7. (35 citations) 10.1038/s42003-020-1037-7](https://doi.org/10.1038/s42003-020-1037-7) [3. (Ashraf2015Two) Tazeen Ashraf, Morag N. Collinson, Joanna Fairhurst, Rubin Wang, Louise C. Wilson, and Nicola Foulds. Two further patients with the 1q24 deletion syndrome expand the phenotype: a possible role for the mir199–214 cluster in the skeletal features of the condition. American Journal of Medical Genetics Part A, 167(12):3153–3160, September 2015. URL: http://dx.doi.org/10.1002/ajmg.a.37336, doi:10.1002/ajmg.a.37336. (17 citations) 10.1002/ajmg.a.37336](https://doi.org/10.1002/ajmg.a.37336) [4. (Wu2022Novel) Zixuan Wu, Xuyan Huang, Minjie Cai, Peidong Huang, and Zunhui Guan. Novel necroptosis-related gene signature for predicting the prognosis of pancreatic adenocarcinoma. Aging, 14(2):869–891, January 2022. URL: http://dx.doi.org/10.18632/aging.203846, doi:10.18632/aging.203846. (50 citations) 10.18632/aging.203846](https://doi.org/10.18632/aging.203846) [5. (Xu2018Genetic) Huaiyuan Xu, Xiaojun Zhu, Hua Bao, Tony Wh Shek, Zongwen Huang, Yongqian Wang, Xue Wu, Yong Wu, Zhili Chang, Shuyu Wu, Qinglian Tang, Huizhong Zhang, Anjia Han, Kenneth Mc Cheung, Changye Zou, Raymond Yau, Wai‐Yip Ho, Gang Huang, Sellma Batalha, Jinchang Lu, Guohui Song, Yao Kang, Yang W. Shao, Ying Lee Lam, Jingnan Shen, and Jin Wang. genetic and clonal dissection of osteosarcoma progression and lung metastasis. International Journal of Cancer, 143(5):1134–1142, May 2018. URL: http://dx.doi.org/10.1002/ijc.31389, doi:10.1002/ijc.31389. (46 citations) 10.1002/ijc.31389](https://doi.org/10.1002/ijc.31389)