RAI16 Blocking Peptide
- Known as:
- RAI16 Blocking Peptide
- Catalog number:
- 33r-3883
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- RAI16 Blocking Peptide
Ask about this productRelated genes to: RAI16 Blocking Peptide
- Gene:
- FAM160B2 NIH gene
- Name:
- family with sequence similarity 160 member B2
- Previous symbol:
- RAI16
- Synonyms:
- FLJ21801
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-07
- Date modifiied:
- 2016-09-30
Related products to: RAI16 Blocking Peptide
Related articles to: RAI16 Blocking Peptide
- This study aimed to develop and validate a prognostic model for metastasis-free survival (MFS) based on genes that may functionally interact with cytotoxic T lymphocytes (CTLs) and M2 macrophages in patients with triple-negative breast cancer (TNBC) who underwent adjuvant radiotherapy. - Source: PubMed
Publication date: 2021/09/05
Ye YunfeiMa JungangZhang QinXiong KaiZhang ZhiminChen ChuanXiao HeWang Dong - Although several causal genes of familial myelodysplastic syndromes (MDS) have been identified, the genetic landscape and the molecular pathogenesis are not totally understood. To explore novel driver genes and their pathogenetic significance, we performed whole-exome sequence analysis of four individuals from a familial MDS pedigree and 10 candidate single-nucleotide variants (C9orf43, CYP7B1, EFHB, ENTPD7, FAM160B2, HELZ2, HLTF, INPP5J, ITPKB, and RYK) were identified. Knockdown screening revealed that Hltf downregulation enhanced colony-forming capacity of primary murine bone marrow (BM) stem/progenitor cells. γH2AX immunofluorescent staining assay revealed increased DNA damage in a human acute myeloid leukemia (AML) cell line ectopically expressing HLTF E259K, which was not observed in cells expressing wild-type HLTF. Silencing of HLTF in human AML cells also led to DNA damage, indicating that HLTF E259K is a loss-of-function mutation. Molecularly, we found that an E259K mutation reduced the binding capacity of HLTF with ubiquitin-conjugating enzymes, methanesulfonate sensitive 2 and ubiquitin-conjugating enzyme E2N, resulting in impaired polyubiquitination of proliferating cell nuclear antigen (PCNA) in HLTF E259K-transduced cells. In summary, our results indicate that a familial MDS-associated HLTF E259K germline mutation induces accumulation of DNA double-strand breaks, possibly through impaired PCNA polyubiquitination. - Source: PubMed
Publication date: 2019/01/29
Takaoka KensukeKawazu MasahitoKoya JunjiYoshimi AkihideMasamoto YosukeMaki HiroakiToya TakashiKobayashi TakashiNannya YasuhitoArai ShunyaUeno ToshihideUeno HironoriSuzuki KenshiHarada HironoriManabe AtsushiHayashi YasuhideMano HiroyukiKurokawa Mineo - Our previous study reported that retinoic acid induced 16 (RAI16) could enhance tumorigenesis in hepatocellular carcinoma (HCC). However, the cellular functions of RAI16 are still unclear. In this study, by immunoprecipitation and tandem (MS/MS) mass spectrometry analysis, we identified that RAI16 interacted with the type II regulatory subunit of PKA (PKA-RIIα), acting as a novel protein kinase A anchoring protein (AKAP). In addition, RAI16 also interacted with heat shock protein 70 (HSP70) and 14-3-3θ. Further studies indicated that RAI16 mediated PKA phosphorylation of HSP70 at serine 486, resulting in anti-apoptosis events. RAI16 was also phosphorylated by the anchored PKA at serine 325, which promoted the recruitment of 14-3-3θ, which, in turn, inhibited RAI16 mediated PKA phosphorylation of HSP70. These findings offer mechanism insight into RAI16 mediated anti-apoptosis signaling in HCC. - Source: PubMed
Ding Cui-LingXu GangTang Hai-LinZhu Shi-YingZhao Lan-JuanRen HaoZhao PingQi Zhong-TianWang Wen