Ask about this productRelated genes to: TMEM38A antibody
- Gene:
- TMEM38A NIH gene
- Name:
- transmembrane protein 38A
- Previous symbol:
- -
- Synonyms:
- MGC3169, TRIC-A
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-12-21
- Date modifiied:
- 2018-08-13
Related products to: TMEM38A antibody
Related articles to: TMEM38A antibody
- TRIC-A is an intracellular cation channel enriched in excitable tissues that is recently identified as a key modulator of sarcoplasmic reticulum (SR) Ca homeostasis through direct interaction with type 2 ryanodine receptors (RyR). Given the intimate anatomical and functional coupling between the SR and mitochondria, we investigated whether TRIC-A contributes to SR-mitochondrial crosstalk under cardiac stress conditions. Using a transverse aortic constriction (TAC) model, we found that TRIC-A mice developed more severe cardiac hypertrophy, underwent maladaptive remodeling, and activated apoptotic pathways compared with wild-type littermates. At the cellular level, TRIC-A-deficient cardiomyocytes were more susceptible to HO-induced mitochondrial injury and displayed abnormal mitochondrial morphology. Live-cell imaging revealed exaggerated mitochondrial Ca uptake during caffeine stimulation and increased propensity for store-overload-induced Ca release (SOICR). Complementary studies in HEK293 cells expressing RyR demonstrated that exogenous TRIC-A expression attenuates RyR-mediated mitochondrial Ca overload, preserves respiratory function, and suppresses superoxide generation. Together, these findings identify TRIC-A as a critical regulator of SR-mitochondrial Ca signaling. By constraining mitochondrial Ca influx and limiting oxidative stress, TRIC-A safeguards cardiomyocytes against SOICR-driven injury and confers protection against pressure overload-induced cardiac dysfunction. - Source: PubMed
Publication date: 2025/10/11
Li AngZhou XinyuPark Ki HoYi JianxunLi XuejunKo Jae-KyunChen YuchenNishi MiyukiYamazaki DaijuTakeshima HiroshiZhou JingsongMa Jianjie - Transmembrane protein 38 (TMEM38) gene family, including TMEM38A and TMEM38B, is responsible for facilitating trimeric intracellular cation transport across the membrane and regulating key cellular processes, such as muscle contraction and cell differentiation in mammals. However, a genome-wide analysis of the chicken TMEM38 gene family, as well as investigations into their biological roles and post-transcriptional expression regulation in fat deposition have not yet been conducted. In this study, we investigated the genome-wide characteristics of chicken TMEM38 gene family, elucidated the regulatory roles of the TMEM38B gene in both abdominal and intramuscular adipogenesis, and explored its miRNA-mediated expression regulatory mechanisms. We found that chicken TMEM38A and TMEM38B exhibited notable conservation in gene structure and motifs across diverse species. Principal component analysis based on SNPs showed that genetic variations in the TMEM38B gene contributed to the selective breeding of commercial broilers. Moreover, gene expression profiling demonstrated that TMEM38A and TMEM38B showed the positive expression in chicken abdominal adipose and muscle tissues, and overall increased expression during the proliferation and adipogenic differentiation of both chicken abdominal and intramuscular preadipocytes. Functionally, TMEM38B overexpression significantly enhanced viability, proliferation, cell cycle progression as well as intracellular triglyceride content and lipid droplet accumulation of both chicken abdominal and intramuscular preadipocytes, paralleling with the expression of proliferative and adipogenic marker genes. Target miRNA prediction identified 37 potential miRNAs targeting the TMEM38B gene. Of these, a dual-luciferase reporter system verified that miR-20b-3p could directly bind to the 3'UTR of the TMEM38B gene and thus inhibit its post-transcriptional expression. Gain-of-function assays showed that miR-20b-3p could suppress the viability, proliferation, and cell cycle progression of chicken abdominal and intramuscular preadipocytes, as well as the adipogenic differentiation of chicken abdominal preadipocytes. Collectively, we demonstrated the promotive effects of TMEM38B in regulating abdominal and intramuscular fat deposition, as well as its post-transcriptional expression inhibition mediated by miR-20b-3p. These findings shed novel lights into the functional role and expression regulation of the miR-20b-3p-TMEM38B axis in adipogenesis, and may provide valuable biomarkers for the genetic improvement of fat traits in chickens. - Source: PubMed
Publication date: 2025/08/16
Li ShuohanCheng XiZhang KeWang YangWei HongyuZhi YihaoCheng ZhiminGuo YulongLi HongTian YadongLiu XiaojunTian Weihua - Clear cell renal cell carcinoma is a prevalent urological malignancy, imposing substantial burdens on both patients and society. In our study, we used bioinformatics methods to select four putative target genes associated with EMT and prognosis and developed a nomogram model which could accurately predicting 5-year patient survival rates. We further analyzed proteome and single-cell data and selected PLCG2 and TMEM38A for the following experiments. Overexpression models of PLCG2 and TMEM38A were generated in Caki-1 and 786-O cell lines using plasmids. The in vitro experiments demonstrated that both of them exerted pro-apoptotic effects on Caki-1 and 786-O cells, inducing G2/M phase arrest, inhibiting proliferation, and suppressing EMT. In summary, we identified potential tumor suppressor factors and stratified ccRCC patients into high-risk and low-risk groups based on these factors. Furthermore, we elucidated the impact of PLCG2 and TMEM38A in Caki-1 and 786-O cell lines, offering novel avenues for therapeutic target exploration. - Source: PubMed
Publication date: 2025/01/25
Zhao YiqiaoYang LiangBai XiaojieDu LuLai HuanLiu YiyangChen PingDiSanto Michael EZhang Xinhua - Radiotherapy plays a crucial role in the management of Cervical cancer (CC), as the development of resistance by cancer cells to radiotherapeutic interventions is a significant factor contributing to treatment failure in patients. However, the specific mechanisms that contribute to this resistance remain unclear. Currently, molecular targeted therapy, including mitochondrial genes, has emerged as a new approach in treating different types of cancers, gaining significant attention as an area of research in addressing the challenge of radiotherapy resistance in cancer. - Source: PubMed
Publication date: 2024/01/24
Wang JiajiaMou XueLu HaishanJiang HaiXian YuejuanWei XilinHuang ZiqiangTang SenlinCen HongsongDong MingyouLiang YuexiuShi Guiling - T-box genes encode transcription factors, which control developmental processes and promote cancer if deregulated. Recently, we described the lymphoid TBX-code, which collates T-box gene activities in normal lymphopoiesis, enabling identification of members deregulated in lymphoid malignancies. Here, we have extended this analysis to cover myelopoiesis, compiling the myeloid TBX-code and, thus, highlighting which of these genes might be deregulated in myeloid tumor types. We analyzed public T-box gene expression datasets bioinformatically for normal and malignant cells. Candidate T-box-gene-expressing model cell lines were identified and examined by RQ-PCR, Western Blotting, genomic profiling, and siRNA-mediated knockdown combined with RNA-seq analysis and live-cell imaging. The established myeloid TBX-code comprised 10 T-box genes, including progenitor-cell-restricted TBX1. Accordingly, we detected aberrant expression of TBX1 in 10% of stem/progenitor-cell-derived chronic myeloid leukemia (CML) patients. The classic CML cell line K-562 expressed TBX1 at high levels and served as a model to identify TBX1 activators, including transcription factor GATA1 and genomic amplification of the TBX1 locus at 22q11; inhibitors, including BCR::ABL1 fusion and downregulated GNAI2, as well as BMP, FGF2, and WNT signaling; and the target genes CDKN1A, MIR17HG, NAV1, and TMEM38A. The establishment of the myeloid TBX-code permitted identification of aberrant TBX1 expression in subsets of CML patients and cell lines. TBX1 forms an integral part of an oncogenic regulatory network impacting proliferation, survival, and differentiation. Thus, the data spotlight novel diagnostic markers and potential therapeutic targets for this malignancy. - Source: PubMed
Publication date: 2023/12/19
Nagel StefanHaake JosephinePommerenke ClaudiaMeyer CorinnaMacLeod Roderick A F