Ask about this productRelated genes to: GDAP1L1 antibody
- Gene:
- GDAP1L1 NIH gene
- Name:
- ganglioside induced differentiation associated protein 1 like 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-15
- Date modifiied:
- 2016-10-05
Related products to: GDAP1L1 antibody
Related articles to: GDAP1L1 antibody
- The purpose of the current study was to examine transcriptomic-based profiling of differentially expressed innate immune genes between indigenous and commercial chickens. In order to compare the transcriptome profiles of the different chicken breeds, we extracted RNA from blood samples of the Isfahan indigenous chicken (as indigenous) and Ross broiler chicken (as commercial) breeds. RNA-Seq yielded totals of 36,763,939 and 31,545,002 reads for the indigenous and commercial breeds, respectively, with clean reads then aligned to the chicken reference genome (Galgal5). Overall, 1327 genes were significantly differentially expressed, of which 1013 genes were upregulated in the commercial versus the indigenous breed, while 314 were more highly expressed in the indigenous birds. Furthermore, our results demonstrated that the and genes were the most significantly expressed genes in the commercial birds and the and genes were the most significant in the indigenous chickens. Of notable finding in this study was that the high-level gene expressions of heat-shock proteins (HSPs) in the indigenous breeds could serve as a guideline for future genetic improvement. This study identified genes with breed-specific expression, and comparative transcriptome analysis helped understanding of the differences in underlying genetic mechanisms between commercial and local breeds. Therefore, the current results can be used to identify candidate genes for further breed improvement. - Source: PubMed
Publication date: 2023/03/25
Sadr Ayeh SadatNassiri MohammadrezaGhaderi-Zefrehei MostafaHeidari MaryamSmith JacquelineMuhaghegh Dolatabady Mustafa - The β-adrenergic receptor (βAR) is found primarily in hearts (mainly in cardiomyocytes [CMs]) and β-arrestin-mediated βAR signaling elicits cardioprotection through CM survival. We showed that microRNA-150 (miR-150) is upregulated by β-arrestin-mediated βAR signaling and that CM miR-150 inhibits maladaptive remodeling post-myocardial infarction. Here, we investigate whether miR-150 rescues cardiac dysfunction in mice bearing CM-specific abrogation of β-arrestin-mediated βAR signaling. Using CM-specific transgenic (TG) mice expressing a mutant βAR (G protein-coupled receptor kinase [GRK]βAR that exhibits impairment in β-arrestin-mediated βAR signaling), we first generate a novel double TG mouse line overexpressing miR-150. We demonstrate that miR-150 is sufficient to improve cardiac dysfunction in CM-specific GRKβAR TG mice following chronic catecholamine stimulation. Our genome-wide circular RNA, long noncoding RNA (lncRNA), and mRNA profiling analyses unveil a subset of cardiac ncRNAs and genes as heretofore unrecognized mechanisms for beneficial actions of βAR/β-arrestin signaling or miR-150. We further show that lncRNA Gm41664 and GDAP1L1 are direct novel upstream and downstream regulators of miR-150. Lastly, CM protective actions of miR-150 are attributed to repressing pro-apoptotic GDAP1L1 and are mitigated by pro-apoptotic Gm41664. Our findings support the idea that miR-150 contributes significantly to βAR/β-arrestin-mediated cardioprotection by regulating unique ncRNA and gene signatures in CMs. - Source: PubMed
Publication date: 2022/12/30
Moukette BrunoKawaguchi SatoshiSepulveda Marisa NHayasaka TaikiAonuma TatsuyaLiangpunsakul SuthatYang LeiDharmakumar RohanConway Simon JKim Il-Man - While psoriasis is known as a T cell- and dendritic cell-driven skin inflammation disease, macrophages are also reported to play some roles in its development. However, the signaling pathway of activated macrophages contributing to psoriasis is not entirely understood. Thus, we aimed to explore the possible mechanisms of how macrophages initiate and sustain psoriasis. The differentiated THP1 cells, stimulated by imiquimod (IMQ), were utilized as the activated macrophage model. IMQ was also employed to produce psoriasis-like lesions in mice. A transcriptomic assay of macrophages revealed that the expressions of pro-inflammatory mediators and GDAP1L1 were largely increased after an IMQ intervention. The depletion of GDAP1L1 by short hairpin (sh)RNA could inhibit cytokine release by macrophages. GDAP1L1 modulated cytokine production by activating the phosphorylation of mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-κB pathways. Besides GDAP1L1, another mitochondrial fission factor, Drp1, translocated from the cytosol to mitochondria after IMQ stimulation, followed by the mitochondrial fragmentation according to the immunofluorescence imaging. Clodronate liposomes were injected into the mice to deplete native macrophages for examining the latter's capacity on IMQ-induced inflammation. The THP1 cells, with or without GDAP1L1 silencing, were then transplanted into the mice to monitor the deposition of macrophages. We found a significant THP1 accumulation in the skin and lymph nodes. The silencing of GDAP1L1 in IMQ-treated animals reduced the psoriasiform severity score from 8 to 2. After depleting GDAP1L1, the THP1 recruitment in the lymph nodes was decreased by 3-fold. The skin histology showed that the GDAP1L1-mediated macrophage activation induced neutrophil chemotaxis and keratinocyte hyperproliferation. Thus, mitochondrial fission can be a target for fighting against psoriatic inflammation. - Source: PubMed
Publication date: 2021/09/27
Alalaiwe AhmedChen Chi-YuanChang Zi-YuSung Jui-TaiChuang Shih-YiFang Jia-You - exhibits anti-inflammatory, antioxidant, and immunomodulatory activities. We aimed to explore the antipsoriatic potential of 2,4-dimethoxy-6-methylbenzene-1,3-diol (DMD) derived from . The macrophages activated by imiquimod (IMQ) were used as the cell model for examining the anti-inflammatory effect of DMD . A significantly high inhibition of IL-23 and IL-6 by DMD was observed in THP-1 macrophages and bone marrow-derived mouse macrophages. The conditioned medium of DMD-treated macrophages could reduce neutrophil migration and keratinocyte overproliferation. DMD could downregulate cytokine/chemokine by suppressing the phosphorylation of mitogen-activated protein kinases (MAPKs) and NF-κB. We also observed inhibition of GDAP1L1/Drp1 translocation from the cytoplasm to mitochondria by DMD intervention. Thus, mitochondrial fission could be a novel target for treating psoriatic inflammation. A psoriasiform mouse model treated by IMQ showed reduced scaling, erythema, and skin thickening after topical application of DMD. Compared to the IMQ stimulation only, the active compound decreased epidermal thickness by about 2-fold. DMD diminished the number of infiltrating macrophages and neutrophils and their related cytokine/chemokine production in the lesional skin. Immunostaining of the IMQ-treated skin demonstrated the inhibition of GDAP1LI and phosphorylated Drp1 by DMD. The present study provides insight regarding the potential use of DMD as an effective treatment modality for psoriatic inflammation. - Source: PubMed
Publication date: 2021/05/14
Chuang Shih-YiChen Chi-YuanYang Shih-ChunAlalaiwe AhmedLin Chih-HungFang Jia-You - Charcot-Marie-Tooth disease (CMT) is one of the most common inherited neurological disorders. Despite the common involvement of ganglioside-induced differentiation-associated protein 1 (GDAP1) in CMT, the protein structure and function, as well as the pathogenic mechanisms, remain unclear. We determined the crystal structure of the complete human GDAP1 core domain, which shows a novel mode of dimerization within the glutathione S-transferase (GST) family. The long GDAP1-specific insertion forms an extended helix and a flexible loop. GDAP1 is catalytically inactive toward classical GST substrates. Through metabolite screening, we identified a ligand for GDAP1, the fatty acid hexadecanedioic acid, which is relevant for mitochondrial membrane permeability and Ca homeostasis. The fatty acid binds to a pocket next to a CMT-linked residue cluster, increases protein stability, and induces changes in protein conformation and oligomerization. The closest homologue of GDAP1, GDAP1L1, is monomeric in its full-length form. Our results highlight the uniqueness of GDAP1 within the GST family and point toward allosteric mechanisms in regulating GDAP1 oligomeric state and function. - Source: PubMed
Publication date: 2021/01/27
Nguyen Giang Thi TuyetSutinen AleksiRaasakka ArneMuruganandam GopinathLoris RemyKursula Petri