Ask about this productRelated genes to: KIAA0247 antibody
- Gene:
- SUSD6 NIH gene
- Name:
- sushi domain containing 6
- Previous symbol:
- KIAA0247
- Synonyms:
- -
- Chromosome:
- 14q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-21
- Date modifiied:
- 2014-12-08
Related products to: KIAA0247 antibody
Related articles to: KIAA0247 antibody
- Gene therapy (GT) using retroviral vectors (RVs) is efficacious in treating monogenic diseases. However, there is an inherent risk for severe adverse effects due to insertional mutagenesis. Preclinical safety assessment and patient monitoring are inevitable in GT. To assess the genotoxic risk of novel RV vectors, mainly murine hematopoietic stem and progenitor cells (HPSCs) are routinely used, because human HSPCs cannot be immortalized in vitro using mutagenic vectors. In this study, we aim to identify early signs of clonal outgrowth by performing integration site analyses (ISA). - Source: PubMed
Publication date: 2026/02/07
Fleischauer JenniJohn-Neek PhilippHa Teng-CheongMansel FriederikeKosanke MaikeSelich AntonHagedorn MaikeBastone Antonella LucíaSchinke MaximilianDziadek ViolettaDittrich-Breiholz Olivervon Kaisenberg ConstantinSchambach AxelRothe Michael - Endometrial receptivity (ERE) is a transient uterine state that determines the success of blastocyst implantation; however, the epigenomic regulation underlying ERE establishment in goats remains unclear. Here, we profiled transcriptional and epigenomic features of endometrial tissues from pregnant goats during the peri-implantation window and nonpregnant control goats in the regressed luteal phase to uncover the transcriptional regulatory networks responsible for ERE establishment in goats, utilizing RNA-seq, ATAC-seq, and H3K27ac CUT&Tag. - Source: PubMed
Publication date: 2026/01/09
Sun ZhipengZhao JunyinLiao YuhaoCheng YuqinYu HoumoWang MingmingFang XingqiangYang SongjianZhao Yongju - The NEDD4-like E3 ubiquitin ligase, WWP2, is involved in a range of host processes from cell differentiation to T cell immunity. Ligase activity is tightly regulated, with WWP2 being held in an autoinhibited state. The binding of a PY motif-containing adaptor, an Ndfip, via the WW domains of NEDD4-like E3 ubiquitin ligases leads to their disinhibition. Here, we show that the canonical Ndfip, NDFIP2, requires multiple PY motifs for interaction with and activation of WWP2. In contrast, the single PY-motif containing Ndfips TMEM127 and SUSD6 functions as a co-disinhibitory pair. TMEM127 and the Salmonella protein SteD also function as a co-disinhibitory pair. However, SteD requires a different region of WWP2, the C2 domain, for interaction with WWP2, and this interaction results in disinhibition of WWP2. These findings demonstrate a range of ways that Ndfips can disinhibit WWP2. To our knowledge, these are the first examples of two Ndfips functioning as co-disinhibitory pairs, and of a bacterial effector that disinhibits an E3 ubiquitin ligase. - Source: PubMed
Publication date: 2025/10/22
Blundell Samkeliso VLiu MeiTocci RominaMajstorovic AndreaTsang SolèneHolden David W - Major histocompatibility complex I (MHC-I) has significant potential for augmenting cancer immunogenicity and immune recognition. Here, we report an innovative therapeutic strategy that synergistically integrates blue light-upregulated MHC-I expression with blue light-induced ferroptosis and cuproptosis. Blue light promoted MHC-I expression in mouse melanoma cells by modulating the NF-κB-SUSD6 signaling axis. Subsequently, an MHC-I-enriched melanoma cytomembrane was used to encapsulate the photoresponsive Cu@ferrihydrite (Cu@Fh) nanoparticles, forming M-Cu@Fh. MHC-I facilitated dendritic cells (DCs) maturation and CD8/CD4 T cells activation. M-Cu@Fh also triggered oxidative stress and concurrent ferroptosis/cuproptosis through the controllable release of Fe/Cu ions under blue-light irradiation. In vivo experiments demonstrated that the combination of blue light and M-Cu@Fh converted immune "cold" tumors into "hot" tumors, suppressed in situ melanoma growth through oxidative damages and enhanced immunogenicity. Furthermore, systemic activation of DCs and CD8/CD4 T cells in lymphoid organs (lymph nodes and spleen) and lungs conferred prophylactic efficacy against abscopal metastasis. Our study elucidates the photoregulatory mechanism of MHC-I in melanoma cells and presents a transformative combinatorial strategy that synergizes blue light-driven photoimmunotherapy (PIT) with blue light-activated photodynamic therapy (PDT) for melanoma management and metastasis prevention. - Source: PubMed
Publication date: 2025/10/01
Yang RongDeng FangqingGao ZiboLi XuHuangfu ShuaiqiTian QingWang HaoyuLiu HuifangWang XuejingChen YaoYang YingchunCheng GenyangZhang Lianbing - A retrovirus inserts its genome into the DNA of a cell, occasionally a germ-line cell that gives rise to descendants of the host organism: it is then called an endogenous retrovirus (ERV). The human genome contains relics from many kinds of ancient ERV. Some relics contributed new genes and regulatory elements. This study finds further kinds of ancient ERV, in the thoroughly-studied human genome version hg38: ERV-Hako, ERV-Saru, ERV-Hou, ERV-Han, and ERV-Goku. It also finds many relics of ERV-V, previously known from just two copies on chromosome 19 with placental genes. It finds a type of ERV flanked by MER41E long terminal repeats (LTRs), with surprisingly little similarity to the known MER41 ERV. ERV-Hako has subtypes that contain sequence from host genes SUSD6 and SPHKAP: the SUSD6 variant was transferred between catarrhine and platyrrhine primates. A retrovirus uses tRNA to prime reverse transcription: Hako is the only human ERV relic that used tRNA-Trp (tryptophan, symbol W), and HERV-W is misnamed because it used tRNA-Arg, based on the Genomic tRNA Database. One ERV-Saru LTR is the previously-described enhancer of AIM2 in innate immunity. This study contributes to understanding primate ERV history, but also shows that related ERVs can have drastic differences, challenging the goal of clearly annotating all ERV relics in genomes. - Source: PubMed
Publication date: 2025/03/13
Frith Martin C