RASGRF1 Control Peptide antibody /CP
- Known as:
- RASGRF1 Control Peptide (anti-) /CP
- Catalog number:
- 'AP12911CP-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- RASGRF1 Control Peptide antibody /
Related genes to: RASGRF1 Control Peptide antibody /CP
- 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 Control Peptide antibody /CP
Related articles to: RASGRF1 Control Peptide antibody /CP
- Colorectal cancer (CRC) remains a major global oncological challenge, largely because most microsatellite-stable (MSS) tumors exhibit intrinsic resistance to immune checkpoint blockade (ICB). Emerging evidence suggests that the gut microbiome and host circadian rhythm jointly regulate mucosal homeostasis; however, their dynamic integration-defined here as the circadian-microbiome-immune axis-remains incompletely understood in CRC. In this review, we synthesize preclinical findings and the limited available clinical evidence concerning this axis. Experimental studies using genetic and lifestyle-related models of circadian disruption indicate that clock dysfunction may impair the intestinal mucosal barrier and alter microbial composition, including depletion of beneficial taxa such as . These changes have been associated with metabolic remodeling, including increased taurocholic acid (TCA), which has been shown in cell and animal models to activate the RasGRF1/MAPK/ERK pathway. Preclinical evidence further suggests that intestinal clock disruption may interact with Wnt signaling and chemokine networks, including CXCL5 and IL-17, thereby promoting the rhythmic recruitment of PD-L1-expressing myeloid-derived suppressor cells (MDSCs). On this basis, we propose the Temporal Immunosuppressive Shield (TIS) as a hypothesis-generating conceptual framework linking epithelial barrier dysfunction, microbial metabolic remodeling, and temporally gated myeloid-mediated suppression of cytotoxic CD8 T cells. Because this integrated model has not yet been directly validated in human MSS CRC, it should not be regarded as an established biological mechanism. We also discuss the potential of biologically phase-aligned ICB and chemotherapy, conceptually termed chronoimmunotherapy, while emphasizing current challenges in circadian biomarker development, interindividual variability, and mouse-to-human translation. Overall, this review outlines a testable spatiotemporal framework and identifies the experimental and clinical studies required to evaluate its relevance to therapeutic resistance in CRC. - Source: PubMed
Publication date: 2026/08/10
Li LiangchenWang Guiying - S. Bido, N. Solari, M. Indrigo, A. D'Antoni, R. Brambilla, M. Morari, and S. Fasano, "Differential Involvement of Ras-GRF1 and Ras-GRF2 in L-DOPA-Induced Dyskinesia," Annals of Clinical and Translational Neurology 2, no. 6 (2015): 662-678, https://doi.org/10.1002/acn3.202. The above article, published online on 24 April 2015 in Wiley Online Library (wileyonlinelibrary.com) has been retracted by agreement between the journal Editor-in-Chief, Ahmet Hoke; American Neurological Association; and John Wiley & Sons, Inc. US. The retraction has been agreed upon following an investigation into concerns raised by a third party. Several image overlaps and duplicated elements in Figures 1, 3, 6, and 7 were identified across different panels even though the corresponding images represent different samples. Accordingly, the editors have lost confidence in the data presented and consider the conclusions of this manuscript insufficiently supported. The authors have been informed of the decision to retract but remained unresponsive. - Source: PubMed
Publication date: 2026/08/20
- 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