Gerbu Adjuvant 3044, for vaccination of sm. animals, Biodegradable liposomes of cationized lipid, emulsifyer WS160 without GMDP
- Known as:
- Gerbu Adjuvant 3044, vaccination sm. animals, Biodegradable liposomes cationized lipid, emulsifyer WS160 GMDP
- Catalog number:
- 3044/5
- Product Quantity:
- 5 ml.
- Category:
- -
- Supplier:
- Accu
- Gene target:
- Gerbu Adjuvant 3044 for vaccination . animals Biodegradable liposomes cationized lipid emulsifyer WS160 without GMDP
Ask about this productRelated genes to: Gerbu Adjuvant 3044, for vaccination of sm. animals, Biodegradable liposomes of cationized lipid, emulsifyer WS160 without GMDP
- Gene:
- SLC25A22 NIH gene
- Name:
- solute carrier family 25 member 22
- Previous symbol:
- -
- Synonyms:
- GC1, FLJ13044, NET44, EIEE3
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-10
- Date modifiied:
- 2016-02-18
Related products to: Gerbu Adjuvant 3044, for vaccination of sm. animals, Biodegradable liposomes of cationized lipid, emulsifyer WS160 without GMDP
Related articles to: Gerbu Adjuvant 3044, for vaccination of sm. animals, Biodegradable liposomes of cationized lipid, emulsifyer WS160 without GMDP
- The brain is uniquely vulnerable to mitochondrial dysfunction, a primary hallmark of neurodegenerative diseases. While mitochondria are universally recognized as cellular powerhouses, their organ-specific functional architectures remain poorly defined. In this study, we present a high-resolution transcriptomic analysis compared across cerebellar tissue (used as the neural reference) and peripheral tissues (heart, kidney, and ovary) to map the coordination of transport, signaling, and detoxification. Using ovarian tissue as a stable physiological baseline, our findings demonstrate that neural mitochondria are fundamentally architected for metabolic surveillance and repair rather than sheer bioenergetic throughput. To safely meet the extreme metabolic demands of synaptic transmission, the brain exhibits reduced transcriptional emphasis on bulk bioenergetic exchange pathways relative to signaling and repair modules in favor of three highly specialized functional pillars: tightly regulated transport (e.g., SFXN4, SLC25A14, and SLC25A22, SLC25A25), highly responsive metabolic signaling (anchored by EFHD1 and retrograde communication), and targeted detoxification and protein repair (e.g., MSRA and MSRB2). Furthermore, phylogenetic conservation analysis comparing the bovine lineage to the human transcriptomic reference data across 90 million years of mammalian evolution confirms that these neural-specific adaptations exhibit highly conserved expression hierarchies. This evolutionary rigidity proves that this specific neurochemical architecture is a deeply conserved, essential requirement for protecting the central nervous system. Consequently, defining this baseline establishes a critical molecular framework for identifying precise therapeutic targets to combat oxidative stress, excitotoxicity, and age-related neurodegeneration. - Source: PubMed
Publication date: 2026/07/17
Sadeesh E MLahamge Madhuri SAmpadi A NMohiddin Roshan - SLC25A22 is a mitochondrial inner membrane glutamate transporter responsible for shuttling glutamate from the cytoplasm into the mitochondrial matrix. Its clinical significance in gastric cancer (GC) remains unclear. GC can be classified into four molecular subtypes: Epstein-Barr virus (EBV)-associated, microsatellite instability (MSI), genomic stability (GS), and chromosomal instability (CIN). In this study, we evaluated the distribution of GC molecular subtypes in Taiwan and examined the association between SLC25A22 expression and patient outcomes. A total of 235 patients with gastric adenocarcinoma treated at Changhua Christian Hospital were included. Tumor subtypes were determined using immunohistochemistry and Epstein-Barr encoding region (EBER) in situ hybridization according to established criteria, and SLC25A22 expression was assessed using an immunohistochemical scoring system. The prevalence of EBV-associated tumors, MMR deficiency (MSI subtype), CIN, and other subtypes was 8.1%, 6.8%, 70.2%, and 14.9%, respectively. EBV-associated tumors showed a relatively lower incidence of metastatic disease (p = 0.014). The median SLC25A22 expression scores were 85 in EBV-associated tumors, 90 in MMR-deficient tumors, 90 in CIN tumors, and 100 in other subtypes. Higher SLC25A22 expression (score > 90) was associated with poorer prognosis (p = 0.014). Our findings indicate that the MSI subtype of GC has a relatively low prevalence in Taiwan and suggest that elevated SLC25A22 expression may serve as a potential biomarker associated with unfavorable prognosis in gastric cancer. Further studies are needed to clarify the biological role of SLC25A22 in tumor progression and therapeutic resistance. - Source: PubMed
Publication date: 2026/03/23
Lee Yu-TingLin Shu-HuiYeh Kun-TuYu Kit-SanHsu Po-YenChan Michael W Y - Genome-wide association studies (GWAS) have identified numerous single nucleotide polymorphisms (SNPs) associated with complex traits in poultry. However, most GWAS-identified variants reside in non-coding regions, making their functional relevance to their phenotypes unclear. Emerging evidence suggests that many of these markers overlap -regulatory elements, yet experimental validation of their biological function remains limited. Here, we investigated non-coding GWAS variants associated with nucleotide-related compounds in chicken breast muscle by targeting SNP-containing genomic regions using a CRISPR activation (CRISPRa) system in DF-1 cells and profiling transcriptomic responses via bulk RNA sequencing to assess the functional impact of activating these regions. Based on chicken muscle-specific epigenetic profiles and chromatin state annotations, we identified three significant GWAS variants on chromosome five associated with nucleotide metabolism. These variants are situated within -regulatory elements, specifically in intron three of , intron one of , and upstream of . To understand their functional impact, we employed an CRISPRa system with targeted guide RNAs to activate each non-coding SNP region in DF-1 cells. This activation resulted in significant changes at the transcriptomic level. Subsequent functional enrichment analysis of the differentially expressed genes consistently highlighted muscle-related pathways across all SNPs, including MAPK signaling, cytoskeletal remodeling, and ECM-receptor interactions, which are potentially involved in regulating nucleotide metabolism and deposition in muscle. Furthermore, transcript-level analysis of RNA-seq reads revealed that the non-coding SNP region within the intron three of may function as an alternative promoter, resulting in significantly higher expression of a shorter transcript that could generate a non-canonical protein isoform. Our study demonstrates that activating genomic regions harboring specific non-coding GWAS SNPs can modulate gene expression, suggesting that these SNPs may contribute to gene regulatory functions. Importantly, this work underscores the powerful utility of CRISPRa as a functional genomics tool for linking GWAS signals to their biological roles in chickens by targeting SNP-containing regions and uncovering consequential molecular phenotypes. - Source: PubMed
Publication date: 2025/10/01
Kim JaewonHan Jeong HoonKim MinjunSchmidt GraceCho EunjinLee Jun HeonKim Tae Hyun - Cervical squamous cell carcinoma(CSCC) represents formidable challenge in clinical oncology, exacerbated by poor prognosis and resistance to current treatments, including anti-PD-1 therapy, highlighting the urgent need for alternative therapeuties. Metabolic characteristics have emerged as potential drivers of treatment resistance and immune evasion. Herein, 1) based on metabolomic and transcriptomic analyses of 44 CSCC and 18 normal tissues, glutamine-enriched and immunosuppressive microenvironment is identified in CSCC. 2) Integrative metabolomic and transcriptomic analyses revealed the glutamine metabolism transporter SLC25A22 as a key mediator in high glutamine metabolism, immune checkpoint activation and CD8+T-cell cytotoxicity. 3) Immunohistochemistry(IHC), multiplex IHC, and flow cytometry validation with clinical CSCC samples revealed not only increased SLC25A22, PD-1 expression and reduced CD8+T-cell cytotoxicity in CSCC but also increased SLC25A22 expression in high PD-L1 expressed CSCC patients, suggesting the potential of targeting SLC25A22 for enhancing CD8+T-cell cytotoxicity and improving anti-PD-1 efficacy, especially in high PD-L1 expressed patients. 4) Novelly, 3D-CSCC organoids are constructed, replicating parental tumor features, and 3D-T-cell-incorporated CSCC organoid models, replicating the interaction between tumor cells and CD8+T cells, for in vitro experiments. 5) Importantly, it is validated through in vitro 3D T-cell-incorporated CSCC organoid models and in vivo animal experiments that targeting the glutamine metabolism transporter SLC25A22, showed promise in enhancing CD8+T-cell cytotoxicity and sensitizing anti-PD-1 therapy. These findings provided insights for future clinical trials exploring metabolic modulation to improve immunotherapy responses in CSCC patients. - Source: PubMed
Publication date: 2025/06/27
Ren TingtingQiu JunjunChen FanghuaJiang QianLiu QinqinWu TongJiang HuaHua Keqin - Epilepsy is a neurological disorder associated with abnormal neuronal activity in the central nervous system, resulting in recurrent seizures. Various anti-seizure medications (ASMs) are effective against epilepsy. However, approximately one-third of patients still do not respond to currently available ASMs either alone or in combination because the etiology of their epilepsy remains unclear. To create a novel zebrafish epilepsy model, we analyzed the exomes of 400 Korean patients with epilepsy via whole-exome sequencing. We found 39 candidate genes and investigated these genes through in situ hybridization and loss-of-function studies, identifying SLC25A22, encoding a mitochondrial glutamate carrier, as a potential epilepsy gene. Subsequently, we generated zebrafish slc25a22a mutants and observed that they displayed spontaneous seizures, high-voltage deflections in local field potentials, and elevated Ca2+ levels propagating from the forebrain to the spinal cord. Of nine ASMs tested, valproic acid (VPA) was able to suppress spontaneous seizure activities in slc25a22a mutant larvae, highlighting the unique anti-seizure effect of VPA in this model. Our findings provide valuable insights into the pathogenesis of epilepsy and suggest slc25a22a as a potential target for novel ASM development. - Source: PubMed
Publication date: 2025/06/20
Lee So-HyunLiang TingChandrasekaran GopalakrishnanZhang JunKim Seong SoonParvathi Sundareswaran VarierLee Seok WonCho Eun-SeoShin Hee-YoungYoon Young-GyuJo JihoonBae Myung AeChoi Seok-YongKim Myeong-Kyu