Ask about this productRelated genes to: RASGRF1 antibody
- Gene:
- RASGRF1 NIH gene
- Name:
- Ras protein specific guanine nucleotide releasing factor 1
- Previous symbol:
- GRF1
- Synonyms:
- CDC25L, CDC25, GRF55, H-GRF55, GNRP, PP13187
- Chromosome:
- 15q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-11
- Date modifiied:
- 2016-10-05
Related products to: RASGRF1 antibody
Related articles to: RASGRF1 antibody
- A growing body of work has linked the dysregulation of transmembrane (TMEM) proteins to the proliferation, metastasis, drug resistance, and tumor microenvironment remodeling of lung cancer, the leading global cause of cancer mortality. Renamed members such as STING1 (stimulator of interferon response cGAMP interactor 1, TMEM173), ANO1 (anoctamin-1, TMEM16A), ORAI1 (ORAI calcium release-activated calcium modulator 1, TMEM142A), ORAI3 (TMEM142C), and NDC1 (NDC1 transmembrane nucleoporin, TMEM48) are among the most extensively studied ones. Mechanisms of TMEM dysregulation in lung cancer span the modulation of Ca influx, lysosomal exocytosis, ferroptosis, Wnt and β-catenin signaling, and immune cell infiltration and immune checkpoint rewiring, among others. Epigenetic silencing and targetable fusions (i.e., TMEM106B-ROS1 and TMEM87A-RASGRF1) create DNA-level vulnerabilities, while miRNA sponges offer RNA-level druggability. A subset of studies revealed context-specific expression (endothelial, B cell, and hypoxic EV) that can be exploited to remodel the tumor microenvironment. One study specifically focused on how isoform-specific expression and localization of TMEM88 determine its functional impact on tumor progression. Yet for most TMEMs, only pre-clinical or early-phase data exist, with many supported by a single study lacking independent validation. This review brings together scattered evidence on TMEM proteins in lung cancer, with the aim of guiding future work on their possible use as biomarkers or therapeutic targets. - Source: PubMed
Publication date: 2026/01/22
Zhang SiweiCao GuojieHu XuelinChen ChenChen Peng - Glioblastoma (GBM) is a lethal brain cancer demanding novel therapeutic targets. This study integrated bioinformatics to identify hub genes and dysregulated pathways in GBM. - Source: PubMed
Publication date: 2025/12/30
Beygi Haniyeh SoheilShahraki AliSheervalilou Roghayeh - : Diffuse large B-cell lymphomas (DLBCLs) are heterogeneous neoplasms. and mutations are associated with the activated B-cell-like (ABC) subtype of DLBCL and often co-occur and lead to constitutive activation of the NF-κB pathway. Several different genetic classifications to date have recognized - and -mutated DLBCLs as a unique subtype with poor response to therapy and unfavorable survival. However, little is known about gene expression in DLBCLs with mutated (and ) in comparison to their wild type counterparts. The objective of this study was to compare the gene expression in DLBCLs according to their mutational status. : A total of 48 primary, treatment-naïve DLBCLs (-mutated: 35%/n = 17, -wild type: 65%/n = 31) were investigated using RNA expression profiling (770 genes), followed by immunohistochemical analysis of the up-regulated genes and survival analysis. : The gene expression analysis revealed that downstream of CD79B and the NF-κB targets , , , and were up-regulated in -mutated DLBCLs. The strongest up-regulation was detected for and . Other up-regulated genes included the apoptosis-related and , as well as genes of cell cycle regulation such as , and . Up-regulation was also found for , , , and the subunit. mutation showed an association with poorer overall survival in a secondary analysis, consistent with prior reports, while survival by / mutation status and the differentially expressed genes showed no significant differences in this cohort. : In conclusion, the current study identified novel up-regulated genes in -mutated DLBCLs beyond NF-κB pathway signaling, which may contribute to a better definition of potential therapeutic targets and further improves the characterization of this distinct and aggressive DLBCL subgroup. - Source: PubMed
Publication date: 2025/11/10
Grossmann LuisJagla WolfgangBettstetter MarcusBertz SimoneSchwarz-Furlan StephanRichter ThomasDechow TobiasDecker ThomasDreyling MartinSotlar KarlBartsch HaraldHartmann ArndtHonecker JuliusGaumann Andreas - The proliferation of fibroblast-like synoviocytes (FLS) and macrophage-mediated inflammation are the main clinical features of rheumatoid arthritis (RA). Studies showed that insulin-like growth factor-2 mRNA binding protein-3 (IGF2BP3) may be involved in regulating the biological functions of different immune cells and FLS. Therefore, the identification of drugs that target IGF2BP3 has important clinical significance for improving RA. Molecular docking and surface plasmon resonance (SPR) analyses were used to identify a small molecule compound targeting IGF2BP3, celastrol (CEL). We subsequently examined the effects of CEL on RAW264.7 cells and FLS. IGF2BP3 knockout (KO) arthritis mice were used to identify the targets and mechanism of CEL in relieving RA. We found that CEL could bind to IGF2BP3 closely and reduce its expression. Additionally, CEL not only inhibited RA-FLS proliferation but also decreased the inflammatory activation of macrophages. The IGF2BP3-RASGRF1-mTORC1 was critical for CEL-mediated amelioration of RA. KO-IGF2BP3 arthritis mice further showed that the protective effect of CEL against arthritis depended on IGF2BP3. Collectively, this study revealed that CEL inhibited the IGF2BP3/RASGRF1/mTORC1 axis to reduce cell proliferation and inflammatory activation, thereby alleviating the progression of RA. Our study suggests that clinical attention should be given to IGF2BP3 inhibitors, such as CEL. - Source: PubMed
Publication date: 2025/10/28
Geng QishunJiao YiDiao WenyaXu JiaheWang ZhaoranWang XingWang ZihanZhao LuYang LeiWang YilinWang KanDeng TingtingWang BailiangXiao Cheng - The impact of genetic variants on high myopia (HM) remains unclear. This study aims to systematically evaluate the relationship between genetic polymorphisms and HM. - Source: PubMed
Publication date: 2026/03/20
Mao BinDong Xing-XuanGong Shi-YiLi Dan-LinFan QiaoPan Chen-Wei