BAK1 antibody - N-terminal region (ARP30473_P050)
- Known as:
- BAK1 (anti-) - N-terminal region (ARP30473_P050)
- Catalog number:
- arp30473_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- BAK1 antibody - N-terminal region (ARP30473_P050)
Related genes to: BAK1 antibody - N-terminal region (ARP30473_P050)
- Gene:
- BAK1 NIH gene
- Name:
- BCL2 antagonist/killer 1
- Previous symbol:
- CDN1
- Synonyms:
- BCL2L7, BAK
- Chromosome:
- 6p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-09
- Date modifiied:
- 2016-02-24
Related products to: BAK1 antibody - N-terminal region (ARP30473_P050)
Related articles to: BAK1 antibody - N-terminal region (ARP30473_P050)
- Liver cancer is one of the most prevalent and lethal cancers worldwide, characterized by poor prognosis and limited treatment options. Triptophenolide (TRI), a diterpenoid compound, has shown anti-proliferative activity in breast and pancreatic cancers, but its role in liver cancer remains largely unexplored. In this study, TRI significantly inhibited the proliferation of HepG2 (hepatoblastoma) and HuH7 (hepatocellular carcinoma) cells in a dose-dependent manner, with IC values decreasing from 279.9 to 229.4 µg/mL (24-48 h) in HepG2 and from 441.1 to 282.6 µg/mL in HuH7. Colony formation assays confirmed the suppression of HCC cell growth. TRI also promoted apoptosis, increasing apoptotic rates to 68.99% in HepG2 and 43.34% in HuH7 at 400 µg/mL (48 h). Cell cycle analysis revealed S-phase arrest, with TRI raising the S-phase population to 42.02% and 45.38%, respectively. Mechanistically, TRI upregulated pro-apoptotic genes (, //, , , , ) and proteins, activating the mitochondrial apoptotic pathway. In vivo, TRI (10 mg/kg) markedly reduced tumor volumes in HepG2 and HuH7 xenografts compared with controls, without obvious systemic toxicity. These findings suggest that TRI exerts anti-proliferative, pro-apoptotic, and cell cycle regulatory effects in HCC. However, further preclinical studies are warranted to elucidate its mechanisms and evaluate its safety profile. - Source: PubMed
Publication date: 2026/04/03
Sabeel ZufaChen RuolanLiu YanChen XiaoyangZhang WenjingPan ShangyangYing LuYu ChangyuanYang Zhao - Cadmium (Cd) is a toxic heavy metal that severely disrupts plant growth, induces oxidative stress and disruption of physiological processes in plants. In this study, we evaluated the potential of two biostimulants, 28-homobrassinolide (28-HBL), a brassinosteroid, and the root endophytic fungus Piriformospora indica, to alleviate Cd-induced stress in Brassica juncea. seedlings. Exposure to Cd significantly impaired seedling morphology and elevated reactive oxygen species (ROS) levels, while biopriming with 28-HBL and root inoculation with P. indica markedly improved morphology and stress resilience. Enzymatic antioxidants (SOD, CAT, APOX, DHAR, MDHAR) and non-enzymatic antioxidants (GSH, phenolics, flavonoids) effectively attenuated ROS levels, with the combined treatment showing the strongest impact. These biochemical enhancements were supported by transcriptional upregulation of antioxidant defense genes. In addition, osmolyte accumulation (proline, glycine betaine [GB]) supported cellular homeostasis under stress. Atomic absorption spectroscopy confirmed reduced Cd uptake in treated seedlings. Notably, P. indica colonization upregulated key brassinosteroid signaling genes (BRI1, BAK1, BES1, and BZR1), suggesting a hormone-mediated mechanism of stress mitigation. The findings highlight a promising synergy between 28-HBL and P. indica, offering an eco-friendly strategy to enhance plant tolerance to Cd stress. - Source: PubMed
Kaur GurvarinderSingh PalampreetMadaan IshaKaushik ShrutiSingh Rajesh KumarSirhindi Geetika - Germ cell tumors (GCTs) are heterogeneous neoplasms arising from primordial germ cells. While genome-wide association studies (GWAS) have identified numerous susceptibility loci for adult testicular GCTs (TGCTs), the heritable basis of pediatric TGCT and GCTs that arise outside the testes remain poorly understood. - Source: PubMed
Publication date: 2026/03/30
Sullivan Shannon MLane JohnStandafer AbigailMcfeeters JamesHubbard Aubrey KLanger Erica KHooten Anthony JRoesler Michelle AGell Joanna JKrailo MarkFrazier A LindsayAmatruda James FPankratz NathanPoynter Jenny N - VDAC2's known role in cancer and immune regulation via enhancing the CD8 T cell-mediated killing, and it is worth systematically digging out the role of VDAC2 in pan-cancer based on this research. Bulk RNA sequencing, single-cell RNA sequencing, and spatial transcriptomic analyses were utilized to explore the role of VDAC2 from multiple perspectives in pan-cancers. RT-PCR, cell co-culture, CCK-8 assay, Transwell invasion assays, and ELISA were performed to validate the expression level and biological function. VDAC2 was upregulated in the majority of pan-cancers, and functional enrichment analyses displayed that VDAC2 may take part in the biological progress of energy metabolism, mitochondrial damage and cell proliferation. The landscape of VDAC2 expression and immune infiltration was constructed, and the VDAC2-BAK1-IFNγ pathway was identified in digestive cancer. VDAC2 had the potential to serve as a novel prognostic, screening cancer indicator and immune therapeutic target sensitive to various drugs. Overexpression of VDAC2 significantly promoted gastric cancer cell proliferation, invasion and immune invasion, as validated in vitro experiments. In short, our pan-cancer analysis constructed a comprehensive landscape of VDAC2's oncogenic role, establishing VDAC2 + -BAK1-IFNγ as an important pathway in tumor progression and immune evasion. VDAC2 emerges not only as a valuable prognostic biomarker but also as a promising novel therapeutic target. - Source: PubMed
Publication date: 2026/03/31
Yan JianingWang JingzhiDong HaotianYe GuoliangShao Yongfu - Abscisic acid (ABA) and brassinosteroid (BR) signaling coordinately regulate plant growth and stress adaptation. Here, we identify the BR pathway component BR signaling kinase (BSK1) to negatively regulate ABA signaling in Arabidopsis. The stability of BSK1 is dynamically controlled by E3 ubiquitin ligases plant U-box 25 (PUB25) and PUB26, which ubiquitinate BSK1 to promote its degradation via the 26S proteasome. This process is likely to be regulated by BR-insensitive 1-associated receptor kinase 1 (BAK1) phosphorylation. Conversely, the deubiquitination enzyme ubiquitin-specific protease 24 (UBP24) stabilizes BSK1 by removing ubiquitin chains. ABA-induced accumulation of PUB25/26 displaces UBP24 from BSK1, permitting BSK1 degradation while redirecting UBP24 to stabilize PUB25/26. This functional pair of E3 ligases (PUB25/26) and deubiquitinase (UBP24), centered on BSK1, plays a vital role in ABA signaling. Our study reveals an evolutionarily conserved paradigm in which the competition between E3 ligases and deubiquitinases spatially orchestrates hormone signaling plasticity. - Source: PubMed
Publication date: 2026/03/27
Li YueyueZhao ZheRen WeiweiZheng HongxiaSun MeihongDai Shaojun