| FAM129A promotes self-renewal and maintains invasive status via stabilizing the Notch intracellular domain in glioma stem cells. | FAM129A promotes self-renewal and maintains invasive status via stabilizing the Notch intracellular domain in glioma stem cells.
Liu G, Zhang P, Chen S, Chen Z, Qiu Y, Peng P, Huang W, Cheng F, Zhang Y, Li H, Xiao Q, Mao F, Wang B, Jiang X, Wan F, Guo D, Yu X., Free PMC Article | 10/5/2023 |
| The negative feedback loop FAM129A/CXCL14 aggravates the progression of esophageal cancer. | The negative feedback loop FAM129A/CXCL14 aggravates the progression of esophageal cancer.
Cao JW, Cui WF, Zhu HJ. | 07/16/2022 |
| MiR-4521 plays a tumor repressive role in growth and metastasis of hepatocarcinoma cells by suppressing phosphorylation of FAK/AKT pathway via targeting FAM129A. | MiR-4521 plays a tumor repressive role in growth and metastasis of hepatocarcinoma cells by suppressing phosphorylation of FAK/AKT pathway via targeting FAM129A.
Ayesha M, Majid A, Zhao D, Greenaway FT, Yan N, Liu Q, Liu S, Sun MZ., Free PMC Article | 03/5/2022 |
| MRNA and protein expression of FAM129A were negatively regulated by miR-135a. | miR-135a deficiency inhibits the AR42J cells damage in cerulein-induced acute pancreatitis through targeting FAM129A.
Zhang KK, Yu SS, Li GY, He L, Liang XQ. | 05/16/2020 |
| Our data suggest that, in normal thyroid cells, FAM129A induces autophagy in order to maintain cell homeostasis and provide substrates under starvation conditions. Instead, in thyroid cancer cells, decreased autophagy may help the cells to overcome cell death. FAM129A regulates autophagy in a cell- and/or context-dependent manner. | FAM129A regulates autophagy in thyroid carcinomas in an oncogene-dependent manner.
Nozima BH, Mendes TB, Pereira GJDS, Araldi RP, Iwamura ESM, Smaili SS, Carvalheira GMG, Cerutti JM. | 03/7/2020 |
| One of the canonical Unfolded protein response branches, through ATF4 and its target gene FAM129A, is required for Prostate cancer growth and thus may serve as a novel therapeutic target. | Regulation of the unfolded protein response through ATF4 and FAM129A in prostate cancer.
Pällmann N, Livgård M, Tesikova M, Zeynep Nenseth H, Akkus E, Sikkeland J, Jin Y, Koc D, Kuzu OF, Pradhan M, Danielsen HE, Kahraman N, Mokhlis HM, Ozpolat B, Banerjee PP, Uren A, Fazli L, Rennie PS, Jin Y, Saatcioglu F. | 02/1/2020 |
| Silencing of Niban in HK-2 cells not only increased the AngII- and endoplasmic reticulum stress-induced apoptosis, but also promoted the expression of caspase 8, caspase 9, Bip, and Chop, suggesting that Niban protein is involved in apoptosis regulation in HK-2 cells, and most likely via caspase-dependent pathway. | Niban protein regulates apoptosis in HK-2 cells via caspase-dependent pathway.
Tang S, Wang J, Liu J, Huang Y, Zhou Y, Yang S, Zhang W, Yang M, Zhang H., Free PMC Article | 01/18/2020 |
| We have shown that FAM129A is associated with variation in clinical asthma steroid responsiveness and that FAM129A modulates steroid responsiveness in lung epithelial cells. | Systems biology and in vitro validation identifies family with sequence similarity 129 member A (FAM129A) as an asthma steroid response modulator.
McGeachie MJ, Clemmer GL, Hayete B, Xing H, Runge K, Wu AC, Jiang X, Lu Q, Church B, Khalil I, Tantisira K, Weiss S., Free PMC Article | 09/21/2019 |
| results suggest a conditional regulation of KRT16 gene by ATF4 that may be inhibited in normal cells, but engaged during cancer progression. Potential roles of KRT16, FAM129A and HKDC1 genes upregulation in adaptive stress responses and pathologies are discussed | Implication of KRT16, FAM129A and HKDC1 genes as ATF4 regulated components of the integrated stress response.
Evstafieva AG, Kovaleva IE, Shoshinova MS, Budanov AV, Chumakov PM., Free PMC Article | 03/17/2018 |
| Data suggest that decreasing C1orf24 protein levels by restoring microRNA miR-106b function may have therapeutic implications. | microRNA-106b-mediated down-regulation of C1orf24 expression induces apoptosis and suppresses invasion of thyroid cancer.
Carvalheira G, Nozima BH, Cerutti JM., Free PMC Article | 08/6/2016 |
| DDIT3, STT3A, ARG2 and FAM129A immunohistochemistry does not appear to be useful in the diagnosis of thyroid follicular neoplasias, as they do not reliably distinguish follicular thyroid carcinoma from follicular thyroid adenoma. | The new molecular markers DDIT3, STT3A, ARG2 and FAM129A are not useful in diagnosing thyroid follicular tumors.
Sigstad E, Paus E, Bjøro T, Berner A, Grøholt KK, Jørgensen LH, Sobrinho-Simões M, Holm R, Warren DJ., Free PMC Article | 08/4/2012 |
| Gene-expression data suggest a difference in expression between STT3A, Clorf24, and TFF3 in FAs versus carcinomas that may be detected from an FNA sample. Findings must be validated from preoperative FNAs in larger numbers | STT3A, C1orf24, TFF3: putative markers for characterization of follicular thyroid neoplasms from fine-needle aspirates.
Patel MR, Stadler ME, Deal AM, Kim HS, Shores CG, Zanation AM. | 07/2/2011 |
| The expression of Niban frequently begins in the early stages of head and neck squamous carcinoma and remains upregulated throughout the carcinogenic process. Niban may be a good molecular marker of HNSCC. | Frequent expression of Niban in head and neck squamous cell carcinoma and squamous dysplasia.
Ito S, Fujii H, Matsumoto T, Abe M, Ikeda K, Hino O. | 04/12/2010 |
| Observational study of gene-disease association. (HuGE Navigator) | Coeliac disease-associated risk variants in TNFAIP3 and REL implicate altered NF-kappaB signalling.
Trynka G, Zhernakova A, Romanos J, Franke L, Hunt KA, Turner G, Bruinenberg M, Heap GA, Platteel M, Ryan AW, de Kovel C, Holmes GK, Howdle PD, Walters JR, Sanders DS, Mulder CJ, Mearin ML, Verbeek WH, Trimble V, Stevens FM, Kelleher D, Barisani D, Bardella MT, McManus R, van Heel DA, Wijmenga C. | 04/1/2009 |
| Niban expression is up-regulated in various types of thyroid tumors. | A novel tumor marker, Niban, is expressed in subsets of thyroid tumors and Hashimoto's thyroiditis.
Matsumoto F, Fujii H, Abe M, Kajino K, Kobayashi T, Matsumoto T, Ikeda K, Hino O. | 01/21/2010 |