CERK polyclonal antibody (A01)
- Known as:
- CERK pab (anti-) (A01)
- Catalog number:
- H00064781-A01
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CERK polyclonal antibody (A01)
Related genes to: CERK polyclonal antibody (A01)
- Gene:
- ABRAXAS2 NIH gene
- Name:
- abraxas 2, BRISC complex subunit
- Previous symbol:
- KIAA0157, FAM175B
- Synonyms:
- Em:AC068896.4, ABRO1
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-16
- Date modifiied:
- 2017-04-27
- Gene:
- AKR1C3 NIH gene
- Name:
- aldo-keto reductase family 1 member C3
- Previous symbol:
- HSD17B5
- Synonyms:
- KIAA0119, DDX, HAKRB, PGFS
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-29
- Date modifiied:
- 2016-10-05
- Gene:
- ARHGAP4 NIH gene
- Name:
- Rho GTPase activating protein 4
- Previous symbol:
- -
- Synonyms:
- KIAA0131, C1, p115, RhoGAP4, SrGAP4
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-28
- Date modifiied:
- 2015-09-11
- Gene:
- ARHGEF7 NIH gene
- Name:
- Rho guanine nucleotide exchange factor 7
- Previous symbol:
- -
- Synonyms:
- KIAA0142, PIXB, DKFZp761K1021, Nbla10314, DKFZp686C12170, BETA-PIX, COOL1, P85SPR, P85, P85COOL1, P50BP, PAK3, P50
- Chromosome:
- 13q34
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-21
- Date modifiied:
- 2016-10-05
- Gene:
- BCLAF1 NIH gene
- Name:
- BCL2 associated transcription factor 1
- Previous symbol:
- -
- Synonyms:
- KIAA0164, BTF
- Chromosome:
- 6q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-13
- Date modifiied:
- 2017-06-09
Related products to: CERK polyclonal antibody (A01)
Related articles to: CERK polyclonal antibody (A01)
- Hepatocellular carcinoma (HCC) ranks as the third leading cause of cancer-related mortality worldwide. As a first-line targeted agent, the clinical application of lenvatinib (LEN) is constrained by drug resistance. This study elucidated the synergistic antitumor mechanism of the traditional Chinese medicine monomer triptolide (TP) in combination with LEN for HCC therapy. In vitro experiments demonstrated that TP-LEN combination significantly enhanced proliferation inhibition and migration blockade in Hep3B and Huh7 cells, exerting synergistic effects through induction of apoptosis and ferroptosis, characterized by intracellular iron accumulation, elevated reactive oxygen species (ROS) levels, and downregulation of ferroptosis-associated proteins GPX4 and SLC7A11. Mechanistic investigations revealed that TP-LEN combination disrupted sphingolipid metabolism by inhibiting ceramide kinase (CERK), leading to accumulation of ceramide (Cer). CERK overexpression abrogated the antitumor effects of the combination, whereas CERK knockdown potentiated cellular sensitivity. In LEN-resistant cell lines, high CERK expression was correlated with drug resistance, and the CERK inhibitor NVP231 restored sensitivity to LEN. In vivo studies using Huh7 xenograft models showed that TP-LEN combination significantly suppressed tumor growth without causing hepatic or renal dysfunction, accompanied by marked downregulation of CERK, GPX4, and SLC7A11 in tumor tissues. This study confirms that TP enhances LEN sensitivity by targeting the CERK/sphingolipid-ferroptosis axis, providing a novel strategy to overcome HCC resistance. - Source: PubMed
Publication date: 2026/06/24
Qin ChulingXue RuiLuo ShashaCai ShikunYang ChangHuang LingyueLuo YuqinXu SiyuanTang KeChen JianningJia LuluXu HuiminTan Qinyou - Metabolic effects of genetic variation often depend on diet, yet the loci underlying diet-dependent developmental responses remain incompletely defined. Here we combine multi-trait phenotyping of Genetic Reference Panel lines with genome-wide mapping in newly developed Recombinant Populations. High sugar causes genotype- and life-stage-dependent changes in metabolic and life-history traits, with development time emerging as a highly heritable, sugar-sensitive phenotype. Mapping in 16 outbred advanced intercross populations reveals distinct association landscapes under low- and high-sugar diets, with a concentrated low-sugar signal, a more distributed high-sugar pattern, and identified genotype-by-diet loci including , and . Functional perturbation supports diet-dependent effects for several prioritized candidates. Allele-frequency analyses identify operationally defined thrifty-like variants associated with delayed development under high sugar and relatively earlier development under low sugar; these variants are enriched for cell-adhesion, neurodevelopmental, and morphogenetic processes. Together, these results establish an outbred framework for dissecting how dietary sugar remodels the genetic architecture of development time. - Source: PubMed
Publication date: 2026/06/10
Bai YulinShabbir SumairaChen YuyanMorgante FabioLudwig MichaelPark Soo-YoungAcharya MohanLi Yang IAli SabirTrudnak AbigailRajesh MutheshreeKreitman MartinZhuang Xuan - Ceramide kinase (CerK) generates ceramide 1-phosphate (C1P), a bioactive sphingolipid involved in diverse cellular responses, but its role in autophagy is not fully understood. Here, we examined whether the CerK/C1P pathway regulates LC3B expression and autophagosome formation in HeLa cells. Proteomics analysis of cerebellum from Cerk-KO mice identified reduced levels of multiple autophagy-related proteins. In HeLa cells, genetic ablation, siRNA-mediated knockdown, and pharmacological inhibition of CerK consistently reduced LC3B-II levels. This effect was reversed by extracellular C1P and by re-expression of wild-type, but not kinase-dead, CerK, indicating that CerK-generated C1P is required for maintenance of LC3B-II. LC3B-II levels remained lower in CERK-KO cells in the presence of bafilomycin A1, and two-step flux analysis showed that disruption of the CerK/C1P pathway preferentially impaired the LC3B-associated autophagosome formation parameter. MAP1LC3B mRNA and Nrf2 protein levels were reduced in CERK-KO cells, and pharmacological activation of Nrf2 tended to restore MAP1LC3B mRNA levels and significantly increased LC3B-II protein levels. Finally, loss of the CerK/C1P pathway enhanced nutrient starvation-induced apoptotic responses and loss of viability. Together, these results identify the CerK/C1P pathway as a positive lipid signaling mechanism that maintains LC3B expression, supports LC3B-associated autophagosome formation, and promotes cell survival under nutrient-deprived conditions. - Source: PubMed
Publication date: 2026/06/12
Funou HidekiArai NatsukaNakajima ShimonKadowaki RyoNakamaura KentaUzu MiakiHonda TakuyaNakamura Hiroyuki - This study was designed to evaluate the modulating effect of dietary chitosan nanogel (CHNG) on antioxidant status and hepato-renal function in Cyprinus carpio. Fish were allocated into 4 groups, each group consisted of 45 fish in triplicates, where each replicate was represented by an aquarium (15 fish/ aquarium). The prophylactic feeding trial lasted for sixty days, where fish were placed on either control, CHNG0.5%, 1% or 1.5%-supplemented diet, then, growth performance was assessed and serum samples was collected for biochemical and antioxidant assessments. Afterwards, fish in the four experimental groups were challenged with Aeromonas sobria,where clinical signs and mortalities were monitored over the fourteen-day challenge period. Then, tissue sampling was performed in order to assess the histopathological outcomes and hepatic gene expression in different groups. The outcomes revealed enhancement of hepato-renal function including ALT, AST, ALP, creatinine, and urea in CHNG-supplemented fish. The control group revealed a remarkable increase in tissue malondialdehyde (MDA) levels that was inhibited by CHNG supplementation in a level-related pattern. The activities of reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) in liver tissue were significantly elevated in a dose-dependent manner in CHNG-supplemented groups. After A. sobria challenge, the hepatic gene expression showed that dietary supplementation with CHNG induced significant down-regulation of apoptosis-related signaling (cERK-1, JNK, P38, and Casp-8) compared with the control group which was challenged with A. sobria and received a basal diet devoid of CHNG. Interestingly, histopathological investigations showed a notable improvement in CHNG-fortified groups relative to the challenged group. Taken together, CHNG-dietary intervention is a potential candidate for enhancing the resistance to A. sobria infection in Cyprinus carpio. - Source: PubMed
Publication date: 2026/06/04
Alharbi Hanan MMahboub Heba HMansour Yasmine AEzz-Eldin Rasha M MShawky Sherif MOrabi Sahar HIsmail Sameh HKhamis TarekAhmed Shaimaa A A - Ovarian cancer (OV) is the leading cause of mortality among gynecological malignancies, often diagnosed at an advanced stage and prone to recurrence after treatment. In order to improve the prognosis, there is an urgent clinical need to identify novel strategies for early intervention and prognosis prediction. Sphingolipids are both important components of cell membranes and closely related to cell signaling. Key enzymes and intermediates of sphingolipid metabolism have critical roles in regulating biological processes such as proliferation and apoptosis of cancer cells, and some of the anticancer drugs targeting sphingolipid metabolism have already entered into clinical trials. However, the prognostic value of sphingolipid metabolism-related genes (SRGs) in OV remains unclear. This study aims to systematically evaluate the prognostic significance of SRGs in OV and construct a prognostic risk model to improve survival prediction. - Source: PubMed
Publication date: 2026/02/26
Lian XinChang HaoYang YunGuo YichenZhang LeiJia Xuemei