Raf1 (Dominant Negative) Recombinant Adenovirus
- Known as:
- Raf1 (Dominant Negative) Recombinant Adenovirus
- Catalog number:
- ADV-133
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Cell Biolabs
- Gene target:
- Raf1 (Dominant Negative) Recombinant Adenovirus
Related genes to: Raf1 (Dominant Negative) Recombinant Adenovirus
- Gene:
- RAF1 NIH gene
- Name:
- Raf-1 proto-oncogene, serine/threonine kinase
- Previous symbol:
- -
- Synonyms:
- Raf-1, c-Raf, CRAF
- Chromosome:
- 3p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: Raf1 (Dominant Negative) Recombinant Adenovirus
Related articles to: Raf1 (Dominant Negative) Recombinant Adenovirus
- Tovorafenib is an oral, selective, CNS-penetrant, type II inhibitor of BRAF and CRAF. fusions and fusions and amplifications are rare oncogenic drivers in many solid tumors. The phase II DAY101-102a substudy of FIRELIGHT-1 (ClinicalTrials.gov identifier: NCT04985604) investigated the efficacy and safety of tovorafenib monotherapy in recurrent/refractory solid tumors with structural alterations in or . - Source: PubMed
Publication date: 2026/10/02
Vieito MariaCabanas Elena GarraldaMehmi InderjitGaudy-Marqueste CarolineO'Neil Bert HMedina Theresa MBody Amy LArance AnaKummar ShivaaniNajjar Yana GBedard Philippe LRankin AndrewChu CarolineMcKenna ChrisHume StephanieKopp Lisa MLee Jeeyun - Noonan syndrome is an autosomal dominant RASopathy caused by germline gain-of-function variants in the renin-angiotensin system/mitogen-activated protein kinase signalling pathway. Hypertrophic obstructive cardiomyopathy is a serious and potentially fatal manifestation of Noonan syndrome, most characteristically associated with RAF1 and RIT1 variants. Trametinib, a selective MEK1/2 inhibitor, has demonstrated efficacy in Noonan syndrome-associated hypertrophic obstructive cardiomyopathy across several genotypes; however, real-world data pairing distinct genotypes with clinical response-particularly for PTPN11- and RAF1-related disease in older children with prior surgical intervention-remain limited. - Source: PubMed
Publication date: 2026/10/01
Al Hadithi MeenaElsedawy OmarKasem MohamedAlsoufi MahmoudObeidat HeshamErgul Yakup - Despite extensive research, the etiology of metabolic dysfunction-associated steatotic liver disease (MASLD) remains incompletely understood. Through analysis of single-cell RNA sequencing (scRNA-seq) data from murine and human MASLD models, we identify a lipid-associated hepatocyte population and implicate Rab1A as its prominent player. Both global knockout and liver-specific knockdown of Rab1A mitigate western diet-induced hepatic steatosis in adult mice. We further show that knockdown of Rab1A in hepatic cells attenuates lipid accumulation by inducing excessive mitophagy. Mechanistically, Rab1A suppresses Raf-1 activation, thereby inhibiting the MEK/ERK1/2 signaling cascade. Pharmacological inhibition of MEK/ERK1/2 via U0126 reverses lipid depletion and restores mitophagy attenuation in Rab1A-deficient cells. We further demonstrate that ERK1/2 directly interacts with and phosphorylates PINK1 at Ser228, triggering PINK1-Parkin-dependent mitophagy. Critically, pharmacological activation of mitophagy by Urolithin A, or by C16-PAF used as a research tool to engage the ERK1/2/PINK1-Parkin axis, alleviates high-fat diet-induced hepatic steatosis and attenuates MASLD progression in mice. In human MASLD patients, Rab1A expression inversely correlates with activation of the Raf-1/ERK1/2/PINK1 pathway. Collectively, our findings identify the Rab1A/Raf-1/ERK1/2/PINK1 axis as a key regulator of mitophagy and MASLD pathogenesis, and highlight this pathway as a promising target for future therapeutic development. - Source: PubMed
Publication date: 2026/09/27
Zhang LiLi JianhuaZhang HuiluQin QiHuang YichenTian XiaofanSun ChaoLi BinbinWang ZhengxinZhang Xin - Alantolactone is a sesquiterpene lactone that possesses anticancer and anti-inflammatory properties. We previously demonstrated that several sesquiterpenes, including alantolactone, induced the ectodomain shedding of tumor necrosis factor receptor 1 (TNF-R1). In the present study, we investigated the upstream signaling pathway underlying alantolactone-induced TNF-R1 ectodomain shedding. Alantolactone down-regulated the expression of full-length TNF-R1 on the cell surface of human lung adenocarcinoma A549 cells, and this was accompanied by an increase in soluble TNF-R1 in the culture medium. TNF-R1 ectodomain shedding was also detected in human embryonic kidney 293T cells and human fibrosarcoma HT-1080 cells, indicating the conservation of this effect in multiple cell lines. The metalloproteinase inhibitor GM6001 markedly suppressed alantolactone-induced soluble TNF-R1 release and restored cell-surface TNF-R1 expression. Among specific inhibitors targeting mitogen-activated protein kinase (MAPK) signaling pathways, TNF-R1 ectodomain shedding was markedly suppressed by the MAPK/extracellular signal-regulated kinase (ERK) kinase (MEK) inhibitor U0126, whereas the suppressive effects of the c-Jun -terminal kinase (JNK) inhibitor SP600125 or the p38 MAPK inhibitor SB203580 were negligible. Consistent with these results, alantolactone increased phospho-ERK and phospho-RAF1 levels within 60-120 min, while p38 MAPK and JNK were minimally phosphorylated during the 120-min incubation. Collectively, these results indicate that alantolactone-induced TNF-R1 ectodomain shedding is mediated by the activation of the RAF1-ERK signaling pathway. - Source: PubMed
Publication date: 2026/09/17
Yarangsee PiimwaraVu Quy VanMiyake YasunobuKataoka Takao - Cannabinoids are terpenophenolic compounds derived from L. that exert a broad range of biological and pharmacological activities. Increasing evidence highlights their potential as modulators of cancer progression specifically through the suppression of tumor cell growth, angiogenesis, and metastasis across multiple tumor models. This review provides a comprehensive overview of the molecular mechanisms by which natural and synthetic cannabinoids induce regulated cancer cell death. Current evidence demonstrates that cannabinoids regulate multiple forms of cancer cell death, including apoptosis, autophagy-dependent cell death, necroptosis, ferroptosis, and parthanatos. These effects are mediated through complex and interconnected signaling pathways such as TRIB3/AKT/mTORC1, PI3K/AKT/mTOR, MAPK/ERK, NF-κB, ERK/JNK/p38-MAPK, and ceramide/Raf1/ERK/ROS. In addition to their direct antitumor effects, cannabinoids can enhance the efficacy of conventional anticancer therapies through the coordinated regulation of complementary cell death pathways. They also provide clinically relevant supportive benefits in palliative care, alleviating chemotherapy-induced nausea, cachexia, and mood or sleep disturbances. Collectively, these findings identify cannabinoids as promising anticancer agents and therapeutic adjuvants, predominantly in the preclinical setting. However, significant challenges remain regarding their safety, optimal dosing, formulation, and clinical efficacy. Further mechanistic studies, rigorous preclinical research, and well-designed clinical trials are required to establish the translation of cannabinoid-based therapies into precision oncology. - Source: PubMed
Publication date: 2026/08/31
El Moghrabi Alaa AAl Khatib AliCheikh Israa AhmadAl Hage CharbelIsmail DimaZhour MariamMwesigwa PhilipDarwiche Nadine