Ask about this productRelated genes to: GADD45GIP1 antibody
- Gene:
- GADD45GIP1 NIH gene
- Name:
- GADD45G interacting protein 1
- Previous symbol:
- -
- Synonyms:
- PLINP-1, MGC4667, MGC4758, CKBBP2, PRG6, Plinp1, CRIF1, CKbetaBP2
- Chromosome:
- 19p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-30
- Date modifiied:
- 2016-10-05
Related products to: GADD45GIP1 antibody
Related articles to: GADD45GIP1 antibody
- CRIF1 is a multifunctional factor that regulates cell biological processes such as the cell cycle, cell proliferation, and energy metabolism, and it is a new molecule that contributes to the poor prognosis of many malignancies. However, its involvement in breast cancer development is not fully known. - Source: PubMed
Publication date: 2026/05/12
Li YongpingLiu JieZhong MingYu WeipingZhu HongboWang XuetingYuan Hao - In their recent study, Li et al. (2025) propose a novel signaling axis in which GADD45GIP1 promotes osteosarcoma progression by stabilizing RPL35, thereby alleviating endoplasmic reticulum (ER) stress through the PERK/eIF2α pathway. While this work identifies a potentially significant oncogenic mechanism, our analysis highlights several critical aspects that require further elucidation. The central claim-that stabilization of a single ribosomal protein, RPL35, directly and specifically alleviates ER stress-presents a conceptual paradox, as enhanced ribosome biogenesis would typically be expected to increase the proteotoxic load. We explore alternative explanations, including the potential for selective mRNA translation or non-ribosomal functions of RPL35. Furthermore, the therapeutic promise of targeting this pathway is tempered by the challenges of inhibiting protein-protein interactions and the risk of on-target toxicity given the pervasive role of the PERK pathway in normal secretory cells. The model also necessitates validation across the spectrum of osteosarcoma's genetic heterogeneity. This letter critically examines these mechanistic ambiguities and proposes essential experiments to validate the model, assess its therapeutic viability, and define its clinical relevance within the complex landscape of osteosarcoma biology. - Source: PubMed
Publication date: 2026/01/28
Qi LiShengGu QinWenYang DuJiangYe ZhijunLi DongDong - Osteosarcoma, mainly arising from mesenchymal cells, is the most common bone tumor in children and adolescents, with high malignancy and a tendency for metastasis and recurrence. Epithelial cells undergoing epithelial-mesenchymal transition (EMT) often signal the start of tumor metastasis, as they gain mesenchymal characteristics that enhance their migration and invasion capabilities. - Source: PubMed
Publication date: 2025/09/04
Zhou FengXu XuezhengLuo YiLiu JianfanBu Jie - Osteosarcoma, a common and aggressive bone tumor found in adolescents and children, is associated with a poor prognosis. The investigation of new molecular mechanisms is deemed vital for the development of innovative treatments. Transcriptomic survival analysis and single-cell RNA sequencing have identified seven highly expressed genes, including GADD45G interacting protein 1 (GADD45GIP1), that are linked to poor prognosis in patients with osteosarcoma. Tissue arrays, comprising 41 normal and 67 tumor cases, have further confirmed the high expression of GADD45GIP1 in osteosarcoma. Functional tests have demonstrated that the silencing of GADD45GIP1 significantly reduces the migration and proliferation of osteosarcoma cells in vitro and in vivo, while its overexpression has the opposite effect. Mechanistic studies have revealed 263 proteins that potentially interact with GADD45GIP1, identified through immunoprecipitation (IP) and liquid chromatography-tandem mass spectrometry (LC-MS/MS), with RPL35 ranking second among them. Cellular interference with RPL35 has been shown to activate the PERK-eIF2α pathway, increase endoplasmic reticulum (ER) stress, and affect the biological behavior of tumor cells. Additionally, the knockdown of GADD45GIP1 has led to a decrease in RPL35 protein stability and elevated polyubiquitination. Notably, the overexpression of RPL35 has counteracted the decrease in cell vitality induced by GADD45GIP1 knockdown. Thus, the high expression of GADD45GIP1 in osteosarcoma has been shown to inhibit the ubiquitin-mediated degradation of RPL35 and induce ER stress through the activation of the PERK-eIF2α pathway, thereby promoting the progression of osteosarcoma. This indicates that GADD45GIP1 serves as a key driver in the development of osteosarcoma and is a potential target for the prevention and therapy of osteosarcoma. - Source: PubMed
Publication date: 2025/07/02
Li ZhiqiangYu XiaoXu RenjieZhang XiangxinShen JunXu Wei - Hypothalamic proopiomelanocortin (POMC) neurons are sensors of signals that reflect the energy stored in the body. Inducing mild stress in proopiomelanocortin neurons protects them from the damage promoted by the consumption of a high-fat diet, mitigating the development of obesity; however, the cellular mechanisms behind these effects are unknown. Here, we induced mild stress in a proopiomelanocortin neuron cell line by inhibiting . In proopiomelanocortin neurons exposed to high levels of palmitate, the partial inhibition of reverted the defects in mitochondrial respiration and ATP production; this was accompanied by improved mitochondrial fusion/fission cycling. Furthermore, the partial inhibition of resulted in increased reactive oxygen species production, increased fatty acid oxidation, and reduced dependency on glucose for mitochondrial respiration. These changes were dependent on the activity of CPT-1. Thus, we identified a CPT-1-dependent metabolic shift toward greater utilization of fatty acids as substrates for respiration as the mechanism behind the protective effect of mild stress against palmitate-induced damage of proopiomelanocortin neurons. Saturated fats can damage hypothalamic neurons resulting in positive energy balance, and this is mitigated by mild cellular stress; however, the mechanisms behind this protective effect are unknown. Using a proopiomelanocortin cell line, we show that under exposure to a high concentration of palmitate, the partial inhibition of the mitochondrial protein results in protection due to a metabolic shift warranted by the increased expression and activity of the mitochondrial fatty acid transporter CPT-1. - Source: PubMed
Publication date: 2024/04/10
Regina-Ferreira LaraValdivieso-Rivera FernandoAngelim Monara K S CMenezes Dos Reis LarissaFurino Vanessa OMorari JoseaneMaia de Sousa LizandraConsonni Sílvio RobertoSponton Carlos HMoraes-Vieira Pedro MVelloso Lício A