Ask about this productRelated genes to: SDK1 antibody
- Gene:
- SDK1 NIH gene
- Name:
- sidekick cell adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- FLJ31425
- Chromosome:
- 7p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-08
- Date modifiied:
- 2016-10-05
Related products to: SDK1 antibody
Related articles to: SDK1 antibody
- Bladder exstrophy and epispadias complex (BEEC) is one of the most severe congenital malformations of the urogenital tract, significantly impacting continence, sexual function, and renal function. To date, the only recurrent genetic aberration identified is the 22q.11.2 microduplication, but several candidate regions and genes including components of the WNT signaling pathway have been proposed. This study aimed to identify additional genes contributing to the pathogenesis of BEEC and to verify previously suggested candidate genes. We performed trio-based whole genome sequencing on 19 individuals with BEEC and their unaffected parents; of those, five carried earlier reported microdeletions. The genome data was also filtered in silico for variants in 204 candidate genes selected from databases, publications, and in-house findings. Variants were prioritized based on allele frequency and predicted functional impact. In 8 of the 19 trios, our findings highlight members of the ADGR-gene family as novel candidate genes for BEEC, alongside other implicated genes such as TRANK1, CSNK1E, IFT122, SDK1, SDK2, and KIF19 and propose two more CNVs as risk factors for BEEC; on chromosome regions 1p36 and 16p11.2. This study identifies novel candidate genes for BEEC within the ADGR gene family. The results also further implicate a complex molecular background of BEEC. - Source: PubMed
Publication date: 2026/02/10
Nordenskjöld AgnetaAlm SamaraEisfeldt JesperCao JiaAnderberg MagnusBarker GillianMatsson HansHolmdahl GundelaLindstrand AnnaLagerstedt-Robinson Kristina - Pediatric obesity is rising globally, and emerging evidence suggests that sleep timing may influence metabolic health through epigenetic mechanisms. This study investigated epigenome-wide DNA methylation patterns associated with bedtime in children and explored their biological relevance. Children aged 6-10 years were classified as early (≤8:30 PM) or late (>8:30 PM) bedtime groups. Saliva-derived DNA was analyzed using the Illumina Infinium MethylationEPIC BeadChip Array, and the Sparse Wrapper Algorithm (SWAG) was applied to identify differentially methylated loci. A total of 1006 CpG sites, representing 571 unique genes, were significantly associated with bedtime ( < 0.001). Significant methylation differences were observed between early and late bedtime groups, with , , , , , , , , , and showing the most consistent variation. Functional enrichment analyses (Gene Ontology, KEGG, and DisGeNET) conducted on the SWAG-identified gene set revealed enrichment in biological processes including peptidyl-lysin demethylation, regulation of sodium ion transport, DNA repair, and lipo-protein particle assembly. Key KEGG pathways included circadian entrainment, neurotransmission (GABAergic, dopaminergic, and glutamatergic), growth hormone synthesis, and insulin secretion. DisGeNET analysis identified associations with neurodevelopmental disorders and cognitive impairment. Cross-comparison with established sleep and obesity gene sets identified ten overlapping genes(, , , , , , , , , and ). These findings suggest that variations in bedtime during childhood may epigenetically modify genes regulating circadian rhythm, metabolism, neuronal connectivity, and stress response, potentially predisposing to later-life developmental, and metabolic challenges. - Source: PubMed
Publication date: 2025/10/31
Richter ErikaPatel PriyadarshniOzdemir Yagmur YNnyaba Ukamaka VMolinari RobertoBabu Jeganathan RGeetha Thangiah - To systematically explore the potential causal relationships among gene expression, DNA methylation, and chronic obstructive pulmonary disease (COPD) susceptibility using a multi-omics Mendelian randomization (MR) framework, and to further investigate key regulatory genes and methylation sites potentially involved in COPD pathogenesis. - Source: PubMed
Publication date: 2025/10/15
Xue ZhichunXue QingDeng XinyuLi ShuqiLiang PengChen HuilingXue HongFang Guiju - The mitogen-activated protein kinase (MAPK) pathway is a conserved signaling system that responds to extracellular signals and translates them into appropriate cellular responses. While multiple MAPK kinase kinases (MAP3Ks) play a crucial role in the step wise transmission of MAPK signals in response to the pathogen infection, little is known about the function of MAP3K15 (also known as apoptosis signal-regulated kinase 3, ASK3) in viral infection. Here, we provide evidence that shrimp MAP3K15 undergoes phosphorylation and activation during a DNA virus, white spot syndrome virus (WSSV) infection, the activated MAP3K15 interacted with the NF-кB homolog, Dorsal, to promote its nuclear translocation for expression of the coiled-coil-containing C-type lectin (CC-CL) and the viral immediate early (ie) genes. CC-CL then activates the JAK/STAT pathway as the ligand to its membrane receptor Domeless, driving the expression of more ie genes. In addition, the JNK/P38 signaling pathway is also activated to promote viral ie genes expression. Importantly, the viral amplification in a wide range of crustaceans were inhibited and the survival rates of host were improved effectively by suppressing MAP3K15 expression or utilizing SDK1, an inhibitor targeting the active form of MAP3K15, suggesting that the MAP3K15 has a critical and conserved function in viral infection. Taken together, this study elucidates a pivotal role and mechanism of MAP3K15 in DNA virus infection, providing novel insights and potential strategies for the control of WSSV infection in crustaceans aquaculture practice. - Source: PubMed
Publication date: 2025/08/01
Ran Xiao-QinLiu Chen-ChenXu Xue-MeiWu Xin-MengKang Cui-Jie - The presence of IKZF1 deletions has been associated with an increased relapse rate in B-cell precursor acute lymphoblastic leukaemia (BCP-ALL). There is a particular subset of IKZF1 cases called IKZF1 (defined by the co-occurrence of IKZF1 and deletions in CDKN2A/B, PAX5, or the PAR1 region, in the absence of ERG deletions), which is also associated with worse prognosis, but some recent studies have not found major differences between the IKZF1 and IKZF1 groups. Therefore, the IKZF1 group still needs further comprehension and our study aims to characterise the molecular heterogeneity and identify molecular markers exclusively associated with IKZF1. Two independent series of cases (TARGET, n = 125 and GenLAb, n = 60) were evaluated by segregating patients into 3 groups: IKZF1, IKZF1, and IKZF1. Differential expression analyses showed that the membrane protein-coding genes most associated with the IKZF1 group were: KCNA5, GREB1, EPOR, SDK1, and PTPRB. Notably, KCNA5 and GREB1 differential expression levels were validated in the GenLAb validation series. Regarding copy number alterations, we observed a high frequency of VPREB1 deletions in the IKZF1 group, as well as additional exclusive deletions in the CD200 and BTLA genes. Recent research suggests that the importance of the IKZF1 profile varies depending on the genetic subgroup. In this scenario, we found associations between IKZF1 and certain genes in BCP-ALL, being KCNA5 and GREB1 the most promising biomarkers for predicting IKZF1. A deeper understanding of these genetic profiles will allow a better risk assessment and offer precise rationale for therapeutic strategies in BCP-ALL. - Source: PubMed
Publication date: 2024/09/22
Blunck Caroline BarbieriPoubel Caroline PiresLopes Bruno ABarbosa Thayana CMaciel Ana Luiza Tardemda Costa Elaine SobralFigueiredo Ariadne da RochaLand Marcelo G PSchramm Márcia TrindadeIkoma-Coltutato Maura Rosane ValérioGomes Renan GarciaLins Mecneide MendesAguiar Thais FerrazMansur Marcela BragaEmerenciano Mariana