Chst5 (mouse)
- Known as:
- Chst5 (mouse)
- Catalog number:
- Y214168
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Chst5 (mouse)
Related genes to: Chst5 (mouse)
- Gene:
- CHST5 NIH gene
- Name:
- carbohydrate sulfotransferase 5
- Previous symbol:
- -
- Synonyms:
- I-GLCNAC-6-ST, FLJ22167
- Chromosome:
- 16q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-07
- Date modifiied:
- 2018-05-14
Related products to: Chst5 (mouse)
Related articles to: Chst5 (mouse)
- The corneal endothelium maintains corneal transparency and vision. Hereditary corneal dystrophies, including macular corneal dystrophy (MCD), Fuchs endothelial corneal dystrophy (FECD), and congenital hereditary endothelial dystrophy (CHED), cause progressive endothelial dysfunction, for which corneal transplantation is currently the main treatment. We evaluate an adeno-associated virus (AAV)-based gene therapy approach in preclinical models of MCD, FECD, and CHED. A refined intracameral injection method enables uniform endothelial transduction without corneal puncture. A single AAV6 administration supports sustained transgene expression in the corneal endothelium for over 18 months without detectable adverse immune responses. In MCD mice, AAV6-Chst5 reduces corneal opacification and restores keratan sulfate levels. In FECD mice, AAV6-Col8a2 prevents corneal opacity in 87.5% of treated eyes. In the CHED model, AAV6-Slc4a11 resolves corneal edema within 7 days. Single-cell RNA sequencing identifies Wnt5a as a downstream factor associated with MCD pathogenesis. These findings support the therapeutic potential of endothelial-targeted gene delivery for corneal endothelial disorders. - Source: PubMed
Zhang Bi NingQi BenxiangChen ShijiuSu JingLi GuoyunWang XinpingRen ZhongmeiZhang HengruiCheng JunQu JingyuYang YangZhou QingjunCong LinXie Lixin - We recently showed that 6-sulfo sialyl -acetyllactosamine (LacNAc) in -linked glycans recognized by the CL40 antibody is abundant in the pleural mesothelium under physiological conditions and that these glycans undergo complementary synthesis by GlcNAc6ST2 (encoded by ) and GlcNAc6ST3 (encoded by ) in mice. GlcNAc6ST3 is essential for the synthesis of R-10G-positive keratan sulfate (KS) in the brain. The predicted minimum epitope of the R-10G antibody is a dimeric asialo 6-sulfo LacNAc. Whether R-10G-reactive KS/sulfated LacNAc oligosaccharides are also present in the pleural mesothelium was unknown. The question of which GlcNAc6STs are responsible for R-10G-reactive glycans was an additional issue to be clarified. Here, we show that R-10G-reactive glycans are as abundant in the pulmonary pleura as CL40-reactive glycans and that GlcNAc6ST3 is only partially involved in the synthesis of these pleural R-10G glycans, unlike in the adult brain. Unexpectedly, GlcNAc6ST2 is essential for the synthesis of R-10G-positive KS/sulfated LacNAc oligosaccharides in the lung pleura. The type of GlcNAc6ST and the magnitude of its contribution to KS glycan synthesis varied among tissues in vivo. We show that GlcNAc6ST2 is required and sufficient for R-10G-reactive KS synthesis in the lung pleura. Interestingly, R-10G immunoreactivity in KSGal6ST (encoded by ) and C6ST1 (encoded by ) double-deficient mouse lungs was markedly increased. MUC16, a mucin molecule, was shown to be a candidate carrier protein for pleural R-10G-reactive glycans. These results suggest that R-10G-reactive KS/sulfated LacNAc oligosaccharides may play a role in mesothelial cell proliferation and differentiation. Further elucidation of the functions of sulfated glycans synthesized by GlcNAc6ST2 and GlcNAc6ST3, such as R-10G and CL40 glycans, in pathological conditions may lead to a better understanding of the underlying mechanisms of the physiopathology of the lung mesothelium. - Source: PubMed
Publication date: 2024/02/07
Takeda-Uchimura YoshikoIkezaki MidoriAkama Tomoya OIhara YoshitoAllain FabriceNishitsuji KazuchikaUchimura Kenji - Macular corneal dystrophy (MCD) is a progressive, bilateral stromal dystrophic disease that arises from mutations in carbohydrate sulfotransferase 6 (CHST6). Corneal transplantation is the ultimate therapeutic solution for MCD patients. Unfortunately, postoperative recurrence remains a significant challenge. We conducted a retrospective review of a clinical cohort comprising 102 MCD patients with 124 eyes that underwent either penetrating keratoplasty (PKP) or deep anterior lamellar keratoplasty (DALK). Our results revealed that the recurrence rate was nearly three times higher in the DALK group (39.13%, 9/23 eyes) compared with the PKP group (10.89%, 11/101 eyes), suggesting that surgical replacement of the corneal endothelium for treating MCD is advisable to prevent postoperative recurrence. Our experimental data confirmed the robust mRNA and protein expression of CHST6 in human corneal endothelium and the rodent homolog CHST5 in mouse endothelium. Selective knockdown of wild-type Chst5 in mouse corneal endothelium (AC), but not in the corneal stroma, induced experimental MCD with similar extracellular matrix synthesis impairments and corneal thinning as observed in MCD patients. Mice carrying Chst5 point mutation also recapitulated clinical phenotypes of MCD, along with corneal endothelial abnormalities. Intracameral injection of wild-type Chst5 rescued the corneal impairments in AC mice and retarded the disease progression in Chst5 mutant mice. Overall, our study provides new mechanistic insights and therapeutic approaches for MCD treatment by high-lighting the role of corneal endothelium in MCD development. - Source: PubMed
Publication date: 2023/07/11
Zhang Bi-NingQi BenxiangDong ChunxiaoZhang BinCheng JunWang XinLi SuxiaZhuang XiaoyunChen ShijiuDuan HaoyunLi DeweiZhu SujieLi GuoyunCao YihaiZhou QingjunXie Lixin - Keratan sulfate (KS) is a glycosaminoglycan that is enriched in vertebrate cornea, cartilage, and brain. During embryonic development, highly sulfated KS (HSKS) is first detected in the developing notochord and then in otic vesicles; therefore, HSKS has been used as a molecular marker of the notochord. However, its biosynthetic pathways and functional roles in organogenesis are little known. Here, I surveyed developmental expression patterns of genes related to HSKS biosynthesis in embryos. Of these genes, the KS chain-synthesizing glycosyltransferase genes, beta-1,3-N-acetylglucosaminyltransferase () and beta-1,4-galactosyltransferase (), are strongly expressed in the notochord and otic vesicles, but also in other tissues. In addition, their notochord expression is gradually restricted to the posterior end at the tailbud stage. In contrast, carbohydrate sulfotransferase (Chst) genes, , , and , are expressed in both notochord and otic vesicles, whereas , and are confined to otic vesicles. Because the substrate for Chst1 and Chst3 is galactose, while that for others is N-acetylglucosamine, combinatorial, tissue-specific expression patterns of Chst genes should be responsible for tissue-specific HSKS enrichment in embryos. As expected, loss of function of led to loss of HSKS in otic vesicles and reduction of their size. Loss of and resulted in HSKS loss in the notochord. These results reveal that Chst genes are critical for HSKS biosynthesis during organogenesis. Being hygroscopic, HSKS forms "water bags" in embryos to physically maintain organ structures. In terms of evolution, in ascidian embryos, and genes are also expressed in the notochord and regulate notochord morphogenesis. Furthermore, I found that a gene is also strongly expressed in the notochord of amphioxus embryos. These conserved expression patterns of Chst genes in the notochord of chordate embryos suggest that Chst is an ancestral component of the chordate notochord. - Source: PubMed
Publication date: 2023/03/14
Yasuoka Yuuri - Dietary fibers such as fructans have beneficial effects on intestinal health but it is unknown whether they impact goblet cells (GCs). Here we studied the effects of inulin-type fructans (ITFs) and graminan-type fructans (GTFs) with different molecular weights on mucus- and endoplasmic reticulum (ER) stress-related genes in intestinal GCs. To that end, GCs were incubated in the presence of ITFs or GTFs, or ITFs and GTFs + TNFα or the -glycosylation inhibitor tunicamycin (Tm). IL-8 production by GCs was studied as a marker of inflammation. Effects between ITFs and GTFs were compared. We found a beneficial impact of GTFs especially on the expression of . GTF II protects from the TNFα-induced gene expression dysregulation of , , , and . Also, all the studied fructans prevented Tm-induced dysregulation of . Interestingly, only the short chain fructans ITF I and GTF I have anti-inflammatory properties on GCs. All the studied fructans except ITF I decreased the expression of the ER stress-related and . All these benefits were fructan-structure and chain length dependent. Our study contributes to a better understanding of chemical structure-dependent beneficial effects of ITFs and GTFs on gut barrier function, which could contribute to prevention of gut inflammatory disorders. - Source: PubMed
Publication date: 2023/02/06
Fernández-Lainez CynthiaAan de Stegge MyrtheSilva-Lagos Luis AlfredoLópez-Velázquez Gabrielde Vos Paul