Ask about this productRelated genes to: GRLF1 antibody
- Gene:
- ARHGAP35 NIH gene
- Name:
- Rho GTPase activating protein 35
- Previous symbol:
- GRLF1
- Synonyms:
- GRF-1, p190ARhoGAP, P190A, KIAA1722, p190RhoGAP
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-15
- Date modifiied:
- 2018-05-17
Related products to: GRLF1 antibody
Related articles to: GRLF1 antibody
- To explore potential genetic contributors across different subtypes of isolated neural tube defects (NTDs) - acrania-exencephaly-anencephaly sequence (AEAS), spinal dysraphism, and encephalocele - using exome sequencing (ES) in a prenatal cohort, with the goal of gaining insight into the molecular diversity underlying these distinct phenotypes. - Source: PubMed
Publication date: 2026/02/19
Botvinik AdiGlasner Vered OffenReches AdiMiremberg HadasHaratz Karina KrajdenBrill TalMalki LironRozenzwaig MichalYaron YuvalLevy Michal - Regorafenib, a multikinase inhibitor, is widely used to treat hepatocellular carcinoma. However, chemoresistance poses a significant challenge to its long-term efficacy. This study conducted a genome-wide CRISPR/Cas9 knockout screen in liver cancer cell lines to identify key regulators of regorafenib resistance and elucidate the underlying molecular mechanisms. The screen identified ARHGAP35 as a critical negative regulator of regorafenib resistance. ARHGAP35 depletion conferred resistance in HepG2 and Huh7 cells, while regorafenib-resistant variants (HepG2-R and Huh7-R) exhibited decreased ARHGAP35 expression. Reintroducing ARHGAP35 restored drug sensitivity. Further analysis revealed that reduced ARHGAP35 expression facilitated epithelial-mesenchymal transition (EMT) by activating the RhoA signaling pathway. Notably, RhoA inhibition reversed EMT and restored regorafenib sensitivity. These findings highlight ARHGAP35 as a key modulator of regorafenib resistance through RhoA suppression, offering potential therapeutic targets to combat chemoresistance in liver cancer. - Source: PubMed
Publication date: 2025/10/16
Chen KunZhang MiaomiaoLiu YuexinDong ZhengnanLiang YaojiZeng JinzhangLiu Jie - Appendiceal goblet cell carcinoma (GCA) is a rare tumor type that has no known precursor. In our diagnostic practice, we observed co-occurrence of GCA with sessile serrated lesions (SSLs) and low-grade appendiceal mucinous neoplasms (LAMNs). Reviewing clinical archives, we identified 35 in-house resections of GCA, in which six (17%) harbored coincident SSLs or LAMNs. Here, we performed paired next-generation sequencing of adenocarcinomas and the coincident lesions to investigate the possibility of shared clonal relationships. For comparison, we also performed paired sequencing on three conventional appendiceal adenocarcinomas with goblet cell differentiation and coincident SSLs or LAMNs. All nine sequenced SSLs or LAMNs harbored activating KRAS mutations, two with concurrent GNAS mutations. There were no apparent shared somatic alterations between the coincident lesions and the six GCAs, the latter of which harbored alterations in other genes including ARID1A, ERBB2, RHOA, and ARHGAP35. In the three conventional adenocarcinomas, there were shared somatic alterations between the adenocarcinomas and the coincident SSLs or LAMNs, including in KRAS, SMAD4, and TP53. In contrast to conventional adenocarcinoma, GCAs do not evidently arise from KRAS-mutated precursor lesions. Based on our paired sequencing study, GCAs were clonally unrelated to coincident KRAS-mutant SSLs and LAMNs, and the reason for the relatively high prevalence of co-occurring lesions among appendectomies containing GCA remains uncertain. - Source: PubMed
Publication date: 2025/09/19
Bauer Anna HNowak Jonathan ARedston MarkPapke David J - By tissue-selective next-generation sequencing, we showed that adenomyotic epithelium harbored genomic alterations thought to be relevant to the development and progression of adenomyosis, including somatic mutations in several cancer-associated genes with high mutant allele frequencies and the gain of chromosome 1q. Clonal relationships among multiple adenomyotic lesions and the normal uterine endometrium delineate the oligoclonal origin of adenomyosis and the spatial expansion of mutant clones. - Source: PubMed
Publication date: 2025/07/18
Suda KazuakiTakahashi KotaroTamura RyoSaito KyotaYamaguchi ManakoYachida NozomiAdachi SosukeKase HiroakiOkuda ShujiroYoshihara KosukeNakaoka Hirofumi - Accurately identifying whether pulmonary nodules are microinvasive adenocarcinoma or invasive carcinoma (MIA or IC) is clinically significant. This study aims to construct a predictive model for this. - Source: PubMed
Publication date: 2025/03/23
Yang QingjieSun XiaoyanLv ShenghuaLi QingtianLan LinhuiLiu NingquanWang MingyangHan KaibaoFeng Xinhai