CCBL1 Antibody
- Known as:
- CCBL1 Antibody
- Catalog number:
- XW-7897
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CCBL1 Antibody
Related genes to: CCBL1 Antibody
- Gene:
- KYAT1 NIH gene
- Name:
- kynurenine aminotransferase 1
- Previous symbol:
- CCBL1
- Synonyms:
- KATI, GTK
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 1995-09-08
- Date modifiied:
- 2016-04-26
Related products to: CCBL1 Antibody
Related articles to: CCBL1 Antibody
- Fetal development is a critical period that establishes reproductive efficiency and herd performance depending on in-utero epigenetic modifications. Dietary restrictions may affect fetal testis development and the offspring fertility. Several studies have connected genetic instability to circadian cycle disruptions, including epigenetic modifications to melatonin, a key regulator. On day 160 of gestation, 17 male-bearing Brangus heifers were assigned to one of four groups in a 2 × 2 factorial treatment arrangement: adequately fed (ADQ; 100% NRC recommendation, n = 3), nutrient restricted (RES; 60% NRC recommendation, n = 5), or ADQ or RES supplemented with 20 mg/d melatonin (ADQ-MEL, n = 5; RES-MEL, n = 4). On day 240 of gestation, heifers underwent Cesarean sections to collect fetuses and testicular tissues. The fetal testicular tissue was processed and analyzed using the Methyl-MiniSeq Service: Genome-wide bisulfite sequencing (Methyl MiniSeq-GWBS). Sequence reads from Methyl Mini-Seq libraries were identified using standard Illumina platform calling software for methylome profile. RNA-Seq libraries were then sequenced on the Illumina platform for transcriptome profile. The common genes between differentially methylated regions (DMRs) and differentially expressed genes (DEGs) across different treatment groups were identified by an overlap analysis using bedtools v2.31.1. There were 413 DMRs in RES-CON and ADQ-CON testicular tissues, without differential gene expression. Compared with the ADQ-CON group, the ADQ-MEL group showed 411 DMRs and a higher KYAT1 gene expression (P-adj <0.05) without methylation changes. Comparing RES-MEL with RES-CON showed that 9 genes (DAAM1, COL28A1, RPL10, TRPM3, SLIT, ARHGEF40, SYT1, TMEM35B, CSPG4B) were expressed more in the former (P-adj <0.05). The only hypomethylated gene was DAAM1 located on chromosome 10. However, 13 genes (PTPRU, snRNP-E, TMEM59L, MUC5B, ANAPC15, FAM221A, SHCBPiL, PAQR5, PPP4R3C, DTNB, LncRNA, SHANK2, RIC3) showed increased expression in RES-CON vs. RES-MEL without differential methylation alterations, yet there were 370 DMRs. Five genes showed increased expression in RES-MEL compared with ADQ-MEL (P-adj <0.05), including histone H2B on chromosome 23. Two genes (PTPRU, TDRD10) showed increased expression in ADQ-MEL compared with RES-MEL (P-adj <0.05) without affecting methylation and 344 DMRs. In conclusion, dietary melatonin supplementation to nutrient restricted dams may influence fetal development as epigenomic and transcriptomic regulators are altered. - Source: PubMed
El Daous HalaLittlejohn Brittni PContreras-Correa Zully ERajput ShiveeliSidelinger Darcie RKing E HeathArick Mark ALemley Caleb O - Dapagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor, has shown significant therapeutic potential in alleviating Diabetes-associated cognitive dysfunction (DACD). However, its specific effects on microglia remain to be further explored. In this study, a type 2 diabetes mellitus (T2DM) mouse model induced by a high-fat diet/streptozotocin (HFD/STZ) was used. It was found that dapagliflozin could significantly reduce fasting blood glucose levels, alleviate weight loss, and improve cognitive function performance in behavioral tests (Y-maze, Morris water maze, and novel object recognition). Histological and biochemical analyses indicated that dapagliflozin could reduce hippocampal neuronal damage, enhance antioxidant capacity (manifested as increased levels of superoxide dismutase and catalase, and decreased malondialdehyde content), and effectively inhibit neuroinflammation (significantly reduced levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6). Transcriptomic and metabolomic analyses revealed that dapagliflozin rebalanced the kynurenine pathway by down-regulating indoleamine 2,3-dioxygenase (IDO1) and kynurenine monooxygenase (KMO), while up-regulating kynurenic acid transaminase 1 (KYAT1), promoting the transformation of metabolic products from neurotoxic substances (such as 3-hydroxykynurenine and kynurenic acid) to neuroprotective substances (kynurenic acid). Additionally, in vitro experiments in high glucose (HG)-stimulated BV-2 microglia further verified that dapagliflozin exerted anti-inflammatory effects by inhibiting the Toll-like receptor/myeloid differentiation factor 88 (TLR/MyD88) signaling pathway and regulating kynurenine metabolic reprogramming. At the same time, overexpression of KMO reversed these effects. In conclusion, these results reveal the multi-dimensional neuroprotective mechanisms of dapagliflozin in DACD, providing substantial evidence for its potential as a therapeutic agent for diabetes-related cognitive dysfunction. - Source: PubMed
Publication date: 2025/12/24
Jia YanhongPang JiangxiaSun ChenWang PuyunHuang QianqianZhao XueyunZhang Dongming - The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that is thought to play important roles in aging, oxidative stress, and cellular senescence. We have previously shown that the AhR agonist kynurenine (Kyn), a tryptophan metabolite that increases with age, can induce muscle atrophy in young mice. AhR overexpression can also lead to muscle atrophy and neuromuscular junction degradation. Here we utilized existing GEO data sets from skeletal muscles of aged mice to examine the impact of two longevity-related interventions, calorie restriction (CR) or treatment with the drug rapamycin (RM), on the expression of genes in the Kyn-AhR pathway. Data were examined in four skeletal muscles: soleus, gastrocnemius, tibialis anterior and triceps brachii. Results show that AhR expression increased with age in the triceps but was decreased with CR in the soleus and gastrocnemius. RM treatment did not significantly alter AhR expression in any of the four muscles of aged mice. Three enzymes that convert kynurenine to kynurenic acid in skeletal muscle, Kyat1, Kyat3 and Got2/Kyat4, are known to increase with endurance exercise and all three increased significantly with CR in aged skeletal muscle. In contrast, RM treatment did not increase Kyat1 expression in aged muscle and RM significantly decreased Kyat3 expression levels in muscles from aged mice. Together these data point to kynurenine aminotransferases as mediating some of the positive effects of CR on skeletal muscle with aging, and support prior research suggesting that CR and RM modulate different patterns of muscle-specific gene expression. - Source: PubMed
Publication date: 2025/11/20
Hamrick Mark WFulzele SadanandIsales Carlos MMcGee-Lawrence Meghan - Colorectal cancer (CRC) cells exhibit a pronounced dependence on l-glutamine to support anabolic growth, redox balance, and mitochondrial metabolism, a phenomenon known as "glutamine addiction." The canonical glutaminase I pathway is mediated by a liver type glutaminase isozyme (LGA; GLS1), a kidney type glutaminase isozyme (KGA; GLS2), and a shortened form (glutaminase C, GAC). GLS1 and GLS2 convert glutamine to glutamate and subsequently to α-ketoglutarate (α-KG) by glutamate dehydrogenase, fueling the TCA cycle. GLS1 inhibitors, such as CB-839 (Telaglenastat), are under clinical evaluation and shows promise in treatment of CRC, particularly in combination therapies. In addition to the canonical pathway, the glutamine transaminase-ω-amidase (GTωA) pathway, a noncanonical route involving transamination of glutamine to α-ketoglutaramate (KGM) by KYAT1/2 and subsequent hydrolysis by ω-amidase (NIT2), offers metabolic flexibility under hypoxic or nutrient-limited conditions. Preclinical studies suggest that GTωA may compensate for GLS1 inhibition, contributing to therapeutic resistance. This review explores the dual roles of glutamine metabolism in CRC, emphasizing the GTωA pathway as a potentially targetable metabolic route that may contribute to therapeutic resistance. While GLS1 inhibitors are under clinical evaluation, emerging evidence suggests that dual targeting of both pathways may enhance treatment efficacy by overcoming metabolic compensation. Understanding the regulatory mechanisms driving the "glutamine shift" between these pathways is critical for developing effective metabolic interventions in CRC. - Source: PubMed
Publication date: 2025/10/10
Voor Sarah FCooper Arthur J LPinto John T - BACKGROUND AND OBJECTIVE: Patients with schizophrenia exhibit significant interindividual variations in their response to pharmacotherapy, adverse effects, and clinical outcomes. While once-monthly paliperidone palmitate (PP1M) injections can improve treatment adherence and continuity compared with oral formulations, suboptimal therapeutic outcomes are still observed in some patients. Although the mechanisms underlying the variability in efficacy of long-acting injectables (LAIs) remain unclear, studies suggest an association with alterations in plasma protein expression. This study aims to investigate the correlation between interindividual differences in the response to PP1M treatment and changes in plasma protein abundance using proteomic analysis. - Source: PubMed
Publication date: 2025/08/29
Zeng WeiweiLiang FeiqingLin XiaoyingZhang YaoyuanZheng YuanziAli TahirDai HaiBin