ARHGAP26 / OPHN1L (C-term) Clone 'C2C3 antibody
- Known as:
- ARHGAP26 / OPHN1L (C-terminus) Clone 'C2C3 (anti-)
- Catalog number:
- 'GTX117598
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- ARHGAP26 / OPHN1L (C-term) Clone 'C2C3 antibody
Related genes to: ARHGAP26 / OPHN1L (C-term) Clone 'C2C3 antibody
- Gene:
- ARHGAP26 NIH gene
- Name:
- Rho GTPase activating protein 26
- Previous symbol:
- -
- Synonyms:
- GRAF, KIAA0621, OPHN1L, OPHN1L1
- Chromosome:
- 5q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-19
- Date modifiied:
- 2019-04-23
Related products to: ARHGAP26 / OPHN1L (C-term) Clone 'C2C3 antibody
Related articles to: ARHGAP26 / OPHN1L (C-term) Clone 'C2C3 antibody
- Colorectal cancer liver metastasis (CRLM) is the primary cause of CRC-related mortality, with inevitable chemoresistance to targeted therapies and immunotherapy. N-methyladenosine (mA), as a crucial epigenetic regulator of gene expression and cellular physiology, involved in the pathogenesis of CRLM. Precise manipulation of mA modifications could offer a non-pharmacological precision treatment for many diseases. However, the precise editing of mA modification in regulating CRLM progression remains elusive. Here we integrated multi-omics and identified zinc finger and BTB domain-containing 7A (ZBTB7A) as an mA-modified transcription factor that promoted CRLM. Mechanistically, METTL3-mediated mA modification of ZBTB7A facilitated recognition by the mA reader YTHDF1/3 complex, enhancing its translation and expression. This mA-dependent regulation promoted CRLM progression via activation of the ARHGAP26/Rho GTPase signaling axis. Notably, we applied a targeted RNA mA erasure (TRME) system to achieve site-specific demethylation at a single site (mA_site_411666) within ZBTB7A mRNA, without perturbing mA abundance. Temporal demethylation at this site is sufficient to inhibit the CRC cell migration. This study unveils the critical role of the METTL3/ZBTB7A/ARHGAP26 axis in the process of mA-mediated CRLM and positions mA precise editing as a promising therapy in the preclinical treatment of CRLM. - Source: PubMed
Publication date: 2026/08/14
Chen XuenaZhao ShuoLiu BochenFan YujiaQiu HuanluRen LingtongZhang XinruiYan ShuruiAn YachunLi ShirongAn JieWang JinshenHu Huili - Glioblastoma (GBM) is an aggressive brain tumor with limited effective treatment options and poor patient outcomes. This study investigates the antitumor activity and underlying mechanisms of of host defense peptides caerin 1.1 (F1) and caerin 1.9 (F3) in glioblastoma models. F1/F3 treatment inhibited the proliferation of U87 cells and was associated with increased expression of ARHGAP26, suppression of β-catenin signaling pathway, and reduced the expression of downstream targets including MMP2, MMP7, and VEGFA. Cell death is primarily induced through apoptosis-related pathways, while pyroptosis-related and PI3K-related signaling showed more limited alterations. Notably, in immunodeficient NSG mice, F1/F3 altered the tumor immune microenvironment by promoting macrophage infiltration and M1-like polarization but did not significantly inhibit tumor growth. In contrast, in PBMC-humanized NSG mice, F1/F3 significantly suppressed U87 tumor growth and was associated with increased infiltration of macrophages and CD8+ T cells, together with reduced PD-L1 expression. These findings demonstrate that F1/F3 exerts both direct anti-tumor effects and immune-modulatory activities in glioblastoma models. The results support further investigation of caerin peptides as potential immunomodulatory therapeutics for glioblastoma. - Source: PubMed
Publication date: 2026/07/09
Zhong FurongWu JinyiWu HongyinWang YichenXiao FengyunXu BinLi JunjieLuo YuandongFu QuanlanLiu XiaosongWang TianfangNi GuoyingZhang Wei - - Source: PubMed
Publication date: 2025/12/30
Long AichunLi TianyunHuang ChengShi YuweiZhang Cuiwei - BRAF, when mutated at V600E, is a well-known potent early oncogenic driver in papillary thyroid carcinoma (PTC), with potential prognostic and therapeutic implications. Non-V600E mutations are less common and without clear functional or therapeutic significance. One class of non-V600E mutations is BRAF gene fusions, which typically involve the C-terminal kinase domain of BRAF joined to a wide repertoire of potential N-terminal fusion partners. The aim of this study was to employ a sequential algorithmic approach to identify patients with BRAF fusions based on an integrated analysis of histologic, immunohistochemistry (IHC), and molecular (NGS) features of BRAF-rearranged PTCs. Nine patients with PTC previously scrutinized as BRAF V600E negative by IHC were analyzed by NGS. The studied 9 cases showed conventional PTC growth; 2 cases displayed a minor high-grade component (tall cell and hobnailing, < 20%), 1 case qualified as high-grade differentiated thyroid carcinoma (presence of necrosis and mitotic activity > 5 MF/ 2 mm; adjacent conventional PTC was present), and 1 case represented neck (lymph node) recurrence after 10 years. BRAF fusions were detected in all cases (10 different fusion partners: NRF1, MKRN1, MACF1, MTDH1, ARHGAP26, STRBF, FCHSDH2, POM121C, UBAP2L, SND1). To our knowledge, 7 of these fusions have not been reported so far in PTC (NRF1::BRAF, MTDH1::BRAF, ARHGAP26::BRAF, BRAF::STRBF, FCHSDH2::BRAF, BRAF::POM121C, UBAP2L::BRAF). In 3 PTCs, BRAF fusions were sole genomic events. Concurrent TERT (c.-124C > T) mutations were detected in 3 PTCs; pathogenic IGF2 amplification was present in another PTC, in addition to BRAF fusion. Two simultaneous fusions BRAF::STRBF and FCHSDH2::BRAF were found in one case of PTC; two BRAF fusions (BRAF::POM121C; UBAP2L::BRAF) co-existed with 2 FOXO1 fusions (FOXO1::TES, YWHAG::FOXO1) in one PTC. In summary, we report 7 new BRAF fusions in PTC BRAF V600E-WT. Additional clinical research is needed to elucidate the behavior of BRAF fusion-driven thyroid carcinomas and the therapeutic utility of MAPK pathway inhibitors. - Source: PubMed
Publication date: 2026/02/16
McGrath NathanLiang LiBakkar RaniaGernon Thomas JMaghami EllieAfkhami MichelleBell Diana - During evolution, organisms evolve mainly through natural and artificial selection, leaving distinctive signatures on genomic coordinates. Such genomic regions offer valuable insights into the molecular mechanisms that influence quantitative traits. India harbours a diverse buffalo population with Murrah breed exhibiting exceptional milk production and quality, notably a high fat and solids-not-fat content. Therefore, the present investigation focused on exploring selection signatures within the genome of the Murrah buffalo through whole-genome resequencing. A total of 17 472 799 SNPs were identified, which were further utilized for identification of selection signatures using site frequency spectrum-based Tajima's D and Nucleotide Diversity; and linkage disequilibrium-based iHS approaches. A total of 248 regions under selection overlapped with 64 QTLs across various traits (milk, production, reproduction, meat and carcass, health, and exterior) on chromosomes 5, 9, and 17. A majority of the identified QTLs (39) were associated with milk-related traits, with 27 QTLs specifically linked to milk fat content. Notably, genes such as , and mapped within the QTLs under selection are implicated in milk traits, while is associated with growth. Hub genes included 3 (milk); (reproduction); (body confirmation), and (heat tolerance). This study lays the groundwork for targeted breeding efforts aimed at enhancing milk production in buffalo. - Source: PubMed
Surati UtsavNiranjan Saket KPundir Rakesh KumarKoul YmberzalVohra VikasGandham Ravi KumarKumar Amod