Ask about this productRelated genes to: ALG6 antibody
- Gene:
- ALG6 NIH gene
- Name:
- ALG6 alpha-1,3-glucosyltransferase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-15
- Date modifiied:
- 2019-04-23
Related products to: ALG6 antibody
Related articles to: ALG6 antibody
- Coronaviruses (CoVs) constitute a major global health threat, and their replication is inseparable from host factors. Investigating host-virus interactions is critical for elucidating the CoV life cycle. Here, we identify alpha-1,3-glucosyltransferase (ALG6) as an essential host factor for CoV replication. Mechanistically, its catalytic activity governs transmissible gastroenteritis virus (TGEV) replication, and ALG6 knockout (KO) inhibits viral entry by downregulating the receptor aminopeptidase N (ANPEP). Moreover, our results indicate that ALG6 KO triggers endoplasmic reticulum (ER) stress, resulting in suppressed viral replication. Further investigations demonstrate that ALG6 KO predominantly hinders viral replication by triggering downstream autophagy induced by ER stress. Transmission electron microscopy analysis reveals that ALG6 KO disrupts the formation of double-membrane vesicles (DMVs) during the initial stages of viral replication. In summary, our findings underscore the crucial role of ALG6 in the replication of CoVs, presenting a promising avenue for the development of potential therapeutic strategies against future CoV infections. - Source: PubMed
Publication date: 2026/03/17
Fu YananGao MeijieFu ZhenSun LimengSu ZhelinTan YubeiXiang YixinShi YuejunXie ShengsongPeng Guiqing - Molecular characterization of balanced complex chromosomal rearrangements (CCR) aids in understanding the pathophysiological mechanism and corresponding genotype-phenotype correlations. The present case describes a male child with intellectual disability, developmental delay, and dysmorphism. A thorough and sequential genetic evaluation using karyotyping, fluorescence in situ hybridization (FISH), chromosomal microarray (CMA), and long read sequencing (LRS) identified a genomically balanced CCR. The CCR involved eight chromosomes, the largest to be documented till date for chromoanagenesis and being balanced despite the high level of complex chromosomal involvement. Translocations accounted for the majority of the rearrangements along with an insertion, inversion, and a small deletion likely driven by chromoplexy. Although the CCR was genomically balanced, it may still result in functionally significant genomic consequences including gene disruptions, gene fusions, and position effects. Long read whole genome sequencing using PacBio was used for breakpoint characterization that revealed three protein-coding genes to be disrupted, namely, NLGN4X, LAMA4, and ALG6. Of these, a candidate association was observed for the NLGN4X gene with the intellectual disability phenotype reported in the proband, which is likely due to disruption of transcription and nonsense mediated decay. We show combinatorial application of advanced genomic technologies with orthogonal cytogenetic techniques in delineating balanced CCRs and understanding the biological and potential clinical implications of balanced yet functionally disruptive CCRs. - Source: PubMed
Publication date: 2026/02/27
Sheth FrennyShah JhanviMuranjan MamtaLiehr ThomasPadutsch NiklasMane SrikantNg Sok Meng EvelynLi PeiningDesai ManishaKansara HenySheth Jayesh JSheth Harsh - - Source: PubMed
Matsuura RyukiKikuchi KenjiroOba AzusaOhashi HirofumiOkamoto Nobuhiko - Transmissible gastroenteritis virus (TGEV) represents a significant threat to global swine production. In the absence of effective antiviral therapies, control relies primarily on vaccination. To identify potential therapeutic targets, we performed a genome-wide CRISPR/Cas9 screen in porcine IPEC-J2 cells, which revealed asparagine-linked glycosylation 5 (ALG5), asparagine-linked glycosylation 6 (ALG6), neurofibromin 2 (NF2), and fucosyltransferase 8 (FUT8) as essential host factors for TGEV infection. Functional characterization demonstrated that ALG5, ALG6, and NF2 knockout impaired viral adsorption and internalization through disruption of aminopeptidase N (pAPN) transcription or N-glycosylation. Consistently, tunicamycin-mediated inhibition of N-glycosylation suppressed TGEV infection. In contrast, FUT8 knockout specifically affects viral internalization and early replication by preventing the formation of double-membrane vesicles (DMVs) but does not affect pAPN expression. This role was independent of FUT8's fucosyltransferase activity, as the enzymatic inhibitor FDW028 had no effect. Mechanistically, we found that FUT8 interacts with the TGEV nonstructural proteins NSP3 and NSP4 to facilitate DMV biogenesis. Our findings delineate distinct mechanisms by which host factors support TGEV infection and provide novel insights for the development of targeted antiviral strategies. - Source: PubMed
Publication date: 2025/11/06
Feng ZhihuaHe XinyanLin MinhuaZhao HengChen YaoChen JianghuaLi ZhaolongShen YangkunChen JianxinYang XiaoyuChen Qi - Atypical chronic lymphocytic leukemia (aCLL) is an indolent lymphoproliferative neoplasm derived from CD19-positive and CD5 or CD23-negative B cells. This paper presents the results of whole genome sequencing (WGS) of lymphoma cells collected from a 29-year-old woman initially diagnosed with aCLL and successfully treated with fludarabine, cyclophosphamide, and rituximab. Eight years later, due to disease progression, she was treated with ibrutinib. After 5 months, her status suddenly deteriorated. PET-CT results suggested Richter transformation (RT). Histopathological examination of nodal lesions confirmed the diagnosis of Diffuse Large B Cell Lymphoma (DLBCL). Finally, the patient was successfully treated with DHAP-R and alloHSCT. WGS of lymphoma cells revealed the presence of pathogenic (COL11A1, MGME1) and likely pathogenic variants (ZMYM3, ALG6, UBA5, and ATG7). Out of these genes, only ZMYM3 is recurrently mutated in B-cell chronic lymphocytic leukemia (B-CLL). The presence of the other lesions requires further studies and indicates the complex molecular background of aCLL transformation to DLBCL. Therefore, the whole-genome variant assessment is worth considering for introduction into a routine procedure at the time of B-CLL diagnosis, especially when RT is suspected. - Source: PubMed
Publication date: 2025/08/09
Przybysz SandraŁojko-Dankowska AnnaRakoczy MagdalenaMarcinkowska-Swojak MałgorzataZeńczak MichałGwóźdź-Bąk KingaHandschuh LuizaLewandowski Krzysztof