C1orf175
- Known as:
- C1orf175
- Catalog number:
- 002869A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- C1orf175
Related genes to: C1orf175
- Gene:
- MROH7 NIH gene
- Name:
- maestro heat like repeat family member 7
- Previous symbol:
- C1orf175, HEATR8
- Synonyms:
- FLJ46354
- Chromosome:
- 1p32.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-21
- Date modifiied:
- 2016-01-22
Related products to: C1orf175
Related articles to: C1orf175
- Inflammatory macrophages (M1 macrophages) and interleukin-1β (IL-1β) serve as critical mediators of inflammatory response and antimicrobial defense in the immune system. Our preliminary investigation identified the HEAT repeat protein (maestro heat-like repeat family member 7, MROH7) as a potential regulator of IL-1β; however, its function in macrophages remains unexplored. In this study, we demonstrated that MROH7 inhibits IL-1β production in M1 macrophages. Mechanistically, MROH7 facilitates the acetylation of lipopolysaccharide-binding protein (LBP) through accumulating intracellular arachidonic acid (AA), thereby promoting its degradation and inhibiting the nuclear factor κB (NF-κB) signaling pathway. Additionally, mice with the myeloid depletion of Mroh7 exhibit an aggravated inflammatory response in lipopolysaccharide (LPS)-induced systemic inflammation. In summary, our study establishes MROH7 as a regulator in macrophage-mediated inflammation, providing critical insights into potential therapeutic targets for inflammatory disorders. - Source: PubMed
Publication date: 2026/02/03
Zhang HangchaoFu JianGuo YanLiu ShijieMei XuehuaZeng XiuRen Wenkai - More than 1200 genes have been shown in the database to be expressed predominantly in the mouse testes. Advances in genome editing technologies such as the CRISPR/Cas9 system have made it possible to create genetically engineered mice more rapidly and efficiently than with conventional methods, which can be utilized to screen genes essential for male fertility by knocking out testis-enriched genes. Finding such genes related to male fertility would not only help us understand the etiology of human infertility but also lead to the development of male contraceptives. In this study, we generated knockout mice for 12 genes (Acrv1, Adgrf3, Atp8b5, Cfap90, Cfap276, Fbxw5, Gm17266, Lrrd1, Mroh7, Nemp1, Spata45, and Trim36) that are expressed predominantly in the testis and examined the appearance and histological morphology of testes, sperm motility, and male fertility. Mating tests revealed that none of these genes is essential for male fertility at least individually. Notably, knockout mice for Gm17266 showed smaller testis size than the wild-type but did not exhibit reduced male fertility. Since 12 genes were not individually essential for male fertilization, it is unlikely that these genes could be the cause of infertility or contraceptive targets. It is better to focus on other essential genes because complementary genes to these 12 genes may exist. - Source: PubMed
Publication date: 2024/04/29
Suzuki AkiraYabuta NorikazuShimada KeisukeMashiko DaisukeTokuhiro KeizoOyama YukiMiyata HaruhikoGarcia Thomas XMatzuk Martin MIkawa Masahito - Ginsenosides have antioxidant and anti-inflammatory features. This study aimed to evaluate the biologic effects of ginsenoside Rb2 pretreatment on ventilator-induced lung injury (VILI) in rats. - Source: PubMed
Publication date: 2020/11/23
Cho Woo HyunKim Yun HakHeo Hye JinKim DohyungKwak Tae WonKim Kwang HoYeo Hye Ju - Apoptosis of vascular endothelial cells (VEC) is the main form of vascular injury that is closely linked to numerous cardiovascular diseases. Therefore, it is important to find new factors that can suppress VEC apoptosis. By using long noncoding RNA (lncRNA) microarray analysis, we found a new read-through lncRNA, MROH7-TTC4, which acted as an apoptosis inhibitor in VECs. Furthermore, by using the inhibitor (ABO) of annexin A7 (ANXA7) GTPase, we discovered that ANXA7 translocated into nucleus and interacted with 5'→3' exoribonuclease (XRN2). The decreased XRN2 phosphorylation induced by ANXA7 GTPase activity inhibition, promoted MROH7-TTC4 expression. Moreover, T-cell intracellular antigen-1 (TIA1), a binding protein of MROH7-TTC4, processed it into MROH7 and TTC4 that could inhibit VEC apoptosis. Here, we conclude that inhibiting ANXA7 GTPase activity promotes the interaction of ANXA7 and XRN2 in nucleus, which regulates the read-through transcription of MROH7-TTC4, and TIA1 is responsible for the process of MROH7-TTC4 that inhibits apoptosis through MROH7 and TTC4. - Source: PubMed
Publication date: 2019/08/24
He XiaoyingZhao XuanSu LeZhao BaoxiangMiao Junying