GPD1 polyclonal antibody (A01)
- Known as:
- GPD1 pab (anti-) (A01)
- Catalog number:
- H00002819-A01
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- GPD1 polyclonal antibody (A01)
Related genes to: GPD1 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: GPD1 polyclonal antibody (A01)
Related articles to: GPD1 polyclonal antibody (A01)
- : Pest management strategies rely on insecticides such as deltamethrin (DM), a commonly applied type II pyrethroid. As a natural component of food-associated microflora, inevitably encounters DM residues in crops used for fermentation processes, including dough leavening and winemaking. However, the prolonged effect of DM exposure on yeast fermentation performance and its capacity to remove DM remained unclear. : In this study, was continuously exposed to a non-lethal concentration (10 mg/L) and a low-inhibition toxic concentration (30 mg/L) of DM for 30 days. : Yeast exhibited high removal capacity, removing 98.05 ± 1.2% and 98.28 ± 0.4% of DM at 10 mg/L and 30 mg/L, respectively. Prolonged exposure to DM at both concentrations did not significantly affect biomass formation, glucose consumption, ethanol production, or acetic acid levels. In contrast, glycerol production increased markedly, reaching 1.1 g/L and 1.5 g/L in cultures exposed to 10 mg/L and 30 mg/L DM, respectively. Consistent with these changes, the expression levels of GPD1 and GPD2, which encode rate-limiting enzymes in glycerol biosynthesis, were upregulated in a dose-dependent manner. : Given the fact that is a workhorse for the biotechnological industry and has a wide range of applications, including in the food industry, elevated glycerol production in yeast under DM exposure is noteworthy in terms of yeast-based applications. - Source: PubMed
Publication date: 2026/04/29
Yavuz MustafaYavuz Hakime GülKaya Recep AnilEren OrhanBereketoglu CeyhunTuranli Beste - Alternative polyadenylation (APA) is one of the important post-transcriptional regulatory mechanisms in eukaryotes. It can regulate gene expression by altering the length of the 3' untranslated region (3'UTR), thus influencing the presence of cis-elements. The growth and development of skeletal muscle is a process which is regulated by multiple factors in an orderly manner, but the role of APA in this process remains unclear. - Source: PubMed
Publication date: 2026/05/13
Jin LinyuYao LeiXu HaonanPeng ChengYang YangLi BugaoCao GuoqingLu Chang - Aconitine (AC) ranks among the leading causes of fatal herbal poisoning globally due to its narrow therapeutic window. Although its cardiovascular toxicity has been extensively studied, the precise molecular mechanisms underlying AC-induced central nervous system damage remain unclear. This study aimed to investigate the role of glycerol-3-phosphate dehydrogenase 1 (GPD1) in AC-induced neurotoxicity and to elucidate the underlying metabolic and molecular mechanisms. In a rat model of acute AC poisoning, significant neurological impairments, anxiety-like behaviors, and neuron-specific cell death were observed. Transcriptomic analyses revealed marked metabolic reprogramming following AC exposure, characterized by upregulation of GPD1 and suppression of the peroxisome proliferator-activated receptor gamma (PPARγ) signaling pathway. Mechanistically, AC disrupted GPD1/PPARγ signaling homeostasis, leading to pathological lipid droplet accumulation and mitochondrial dysfunction, as evidenced by loss of membrane potential and ATP depletion, ultimately resulting in neuronal apoptosis. Notably, targeted knockdown of Gpd1 using shRNA alleviated lipid accumulation, restored mitochondrial function, and significantly improved survival rates and neurological outcomes in poisoned rats. These findings identify the aconitine-GPD1-lipid/mitochondrial axis as a key mechanism underlying AC-induced neurotoxicity and suggest GPD1 as a potential therapeutic target. - Source: PubMed
Publication date: 2026/04/29
Jiang ChenHu WenDeng SangyangHuang YongjieWang LinboYang ZhenyuLi YufeiLi PingWu Haiying - - Source: PubMed
Publication date: 2026/04/30
Das SamannayBiswas Tamoghna - Osteoporosis is the leading cause of fractures, characterized by reduced bone formation and increased bone resorption. Exploring the potential mechanisms of antidiabetic drugs in the treatment of OP provides valuable clinical insights for the future pharmacological management of osteoporosis patients. - Source: PubMed
Publication date: 2026/04/21
Jing Yu-LongZhu Xiao-YangGong Shen-AoSun TaoLin Xiao-Yan