C15orf40 Blocking Peptide, Blocking Peptides
- Known as:
- C15orf40 Blocking Peptide, Blocking Peptides
- Catalog number:
- 33R-2270
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- C15orf40 Blocking Peptide Peptides
Related genes to: C15orf40 Blocking Peptide, Blocking Peptides
- Gene:
- C15orf40 NIH gene
- Name:
- chromosome 15 open reading frame 40
- Previous symbol:
- -
- Synonyms:
- MGC29937
- Chromosome:
- 15q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-24
- Date modifiied:
- 2016-09-30
Related products to: C15orf40 Blocking Peptide, Blocking Peptides
Related articles to: C15orf40 Blocking Peptide, Blocking Peptides
- In recent years, liquid-liquid phase separation (LLPS) has garnered increasing attention in the field of oncology. However, its role in osteosarcoma remains largely unexplored. We aimed to construct a prognostic risk model associated with LLPS and to investigate the impact of LLPS-related genes on osteosarcoma briefly. - Source: PubMed
Publication date: 2025/12/29
Huang XinyuXiong LiangZeng JiaxingLi ShanhangCai YangjieZou ZhuanYang MingxiuLi HeningLiu YunHe Maolin - Proximal microdeletions on chromosome 15q25.2 are very rare, and are associated with neurodevelopmental delay, inguinal hernia, chest deformities, and anemia. The minimum length missed so far is 1.4 Mb. However, there were no cases reported till date on microdeletions at position q25.2 on chromosome 15 with premature ovarian failure (POF). - Source: PubMed
Publication date: 2020/09/07
Chen ZhenChen HongYuan KeWang Chunlin - Primary failure of tooth eruption (PFE) is a rare odontogenic defect and is characterized by failure of eruption of one or more permanent teeth. The aim of the study is to identify the genetic defect in a family with seven affected individuals segregating autosomal dominant non-syndromic PFE. Whole genome single-nucleotide polymorphism (SNP) genotyping was performed. SNP genotypes were analysed by DominantMapper and multiple shared haplotypes were detected on different chromosomes. Four individuals, including three affected, were exome sequenced. Variants were annotated and data were analysed while considering candidate chromosomal regions. Initial analysis of variants obtained by whole exome sequencing identified damaging variants in C15orf40, EPB41L4A, TMEM232, KMT2C, and FBXW10 genes. Sanger sequencing of all family members confirmed segregation of splice acceptor site variant (c.1013-2 A > G) in the KMT2C gene with the phenotype. KMT2C is considered as a potential candidate gene based on segregation analysis, the absence of variant in the variation databases, the presence of variant in the shared identical by descent (IBD) region and in silico pathogenicity prediction. KMT2C is a histone methyltransferase and recently the role of another member of this family (KMT2D) has been implicated in tooth development. Moreover, protein structures of KMT2C and KMT2D are highly similar. In conclusion, we have identified that the KMT2C gene mutation causes familial non-syndromic PFE. These findings suggest the involvement of KMT2C in the physiological eruption of permanent teeth. - Source: PubMed
Publication date: 2019/11/11
Assiry Ali AAlbalawi Alia MZafar Muhammad SKhan Siraj DUllah AnharAlmatrafi AhmedRamzan KhushnoodaBasit Sulman