Ask about this productRelated genes to: SRBD1 antibody
- Gene:
- SRBD1 NIH gene
- Name:
- S1 RNA binding domain 1
- Previous symbol:
- -
- Synonyms:
- FLJ10379
- Chromosome:
- 2p21
- Locus Type:
- gene with protein product
- Date approved:
- 2006-03-24
- Date modifiied:
- 2019-03-19
Related products to: SRBD1 antibody
Related articles to: SRBD1 antibody
- : Radioresistance is a critical challenge in the treatment of esophageal squamous cell carcinoma (ESCC). Histone lysine-specific demethylase 4D (KDM4D) has been implicated in DNA damage response; however, its role in regulating ESCC radiosensitivity remained unclear. We hypothesized KDM4D modulates radiosensitivity through the c-Myc/checkpoint kinase 1 (CHK1) pathway. : To investigate the role of KDM4D in ESCC radiosensitivity and to elucidate the underlying molecular mechanisms. : KDM4D expression was analyzed in tumor samples from 32 ESCC patients who received neoadjuvant radiotherapy. ESCC cell lines with KDM4D knockdown or overexpression were subjected to irradiation, and radiosensitivity was evaluated. Chromatin immunoprecipitation-polymerase chain reaction (ChIP-PCR), luciferase assay, and xenograft models were used to explore the underlying mechanisms. : Elevated KDM4D expression was associated with improved response to radiotherapy and prolonged progression-free survival (PFS). KDM4D knockdown significantly reduced radiation-induced apoptosis. Mechanistically, KDM4D promoted the demethylation of histone H3 lysine 9 trimethylation (H3K9me3), thereby activating S1 RNA-binding domain-containing protein 1 (SRBD1). SRBD1 subsequently upregulated ribosomal protein L11 (RPL11), which suppressed c-Myc expression, thereby downregulating wild-type p53-induced phosphatase 1 (WIP1) and CHK1. Rescue experiments and xenograft studies further verified this regulatory axis. : KDM4D enhances ESCC radiosensitivity through the SRBD1/RPL11/c-Myc/WIP1/CHK1 pathway, highlighting its potential as both a diagnostic biomarker and a therapeutic target. - Source: PubMed
Publication date: 2026/05/15
Gao ZhenhuaHan XiaoyunYuan Shuanghu - Identifying genomic regions under selection is crucial for comprehending the evolutionary history of the domestic chicken. Arabian Peninsula (AP) indigenous chickens are mostly found outdoors, being reared alongside other livestock for production purposes. These birds show high resilience to extreme temperatures (hot and cold), typical of the desert environment. The selection pressures responsible for unique local adaptations in these birds remain largely unidentified. Here, we aimed to investigate the genome diversity and structure of 15 indigenous chicken populations including 13 populations from the AP (n = 5), Ethiopia (n = 6), and the People's Republic of China (n = 2). We also included two commercial chicken populations, Fayoumi (selected for heat tolerance) and Chantecler (known for its cold tolerance). Principal component (PC) analysis separated all the populations based on their geographic areas of origin. PC1 separates the Ethiopian populations from the Chinese and AP populations, while PC2 separates the AP populations from the Chantecler, and the Ethiopian populations from the Dulong and Chantecler. The genome-wide signatures of analyses identified many candidate regions under positive selection. They include genes that may be associated with thermotolerance. These are involved in energy balance and metabolism (SUGCT, HECW1, MMADHC), cells apoptosis (APP, SRBD1, NTN1, PUF60, SLC26A8, DAP, SUGCT), angiogenesis (RYR2, LDB2, SOX5), skin protection to solar radiation (FZD10, BCO2, WNT5B, COL6A2, SIRT1) as well as growth (NELL1). Our findings suggest that Arabian chicken populations have a distinct gene pool polymorphism in relation to their adaptation to the harsh climatic environments of the AP. - Source: PubMed
Assiri AbdulwahadVallejo-Trujillo AdrianaAl-Abri MohammedBahbahani HussainAlmathen FaisalAhbara AbulgasimAl Marzooqi WaleedTijjani AbdulfataiLawal RamanHanotte Olivier - Despite significant progress made in functional genomics, the roles of a relatively small number of essential genes remain enigmatic. Here, we characterize S1 RNA-binding domain-containing protein 1 (SRBD1), an essential gene with no previously assigned function. Through genetic, proteomic, and functional approaches, we discovered that SRBD1 is a DNA-binding protein and a key component of the mitotic chromatid axis. The loss of SRBD1 results in a pronounced defect in sister chromatid segregation that strikingly resembles the phenotype observed when sister chromatid decatenation is perturbed by topoisomerase IIα (TOP2A) dysfunction. Using genetic screens, we uncovered that the requirement for SRBD1 depends on the presence of condensin II but not condensin I. Moreover, we found that SRBD1 activity is most critical during prophase, when chromosome condensation is established. Taking these results together, we propose that SRBD1 acts during prophase to safeguard the decatenation process to prevent the formation of difficult-to-resolve DNA structures, thereby averting severe chromosome missegregations. - Source: PubMed
Publication date: 2025/03/18
Raaijmakers Jonne AJanssen Louise M EMazouzi AbdelghaniHondema Amber L HBorza RazvanFish AlexanderElbatsh Ahmed M OKazokaitė-Adomaitienė JustinaVaquero-Siguero NuriaMayayo-Peralta IsabelNahidiazar LeilaFriskes AnoekHoekman LiesbethBleijerveld Onno BHoencamp ClaireMoser Sarah CJonkers JosJalink KeesZwart WilbertCelie Patrick H NRowland Benjamin DPerrakis AnastassisBrummelkamp Thijn RMedema René H - Accurate sister chromatid segregation requires remodeling chromosome architecture, decatenation, and attachment to the mitotic spindle. Some of these events are initiated during S-phase, but they accelerate and conclude during mitosis. Here we describe SRBD1 as a histone and nucleic acid binding protein that prevents DNA damage in interphase cells, localizes to nascent DNA during replication and the chromosome scaffold in mitosis, and is required for chromosome segregation. SRBD1 inactivation causes micronuclei, chromatin bridges, and cell death. Inactivating SRBD1 immediately prior to mitotic entry causes anaphase failure, with a reduction in topoisomerase IIα localization to mitotic chromosomes and defects in properly condensing and decatenating chromosomes. In contrast, SRBD1 is not required to complete cell division after chromosomes are condensed. Strikingly, depleting condensin II reduces the severity of the anaphase defects in SRBD1-deficient cells by restoring topoisomerase IIα localization. Thus, SRBD1 is an essential genome maintenance protein required for mitotic chromosome organization and segregation. - Source: PubMed
Publication date: 2025/02/16
Lovejoy Courtney AWessel Sarah RBhowmick RahulHatoyama YukiKanemaki Masato TZhao RunxiangCortez David - Low expression of certain ribosomal proteins leads to the inactivation of p53, which is mediated mainly by RPL5 or RPL11 (ribosomal protein L11). It is also unknown what mechanisms drive aberrant ribosomal proteins expression in tumor. SRBD1 (S1 RNA-binding domain 1), as a highly conserved RNA-binding protein, is lowly expressed in glioma tissues and correlated with glioma prognosis. In this study, we observed that SRBD1 was closely related to p53 signaling. The upregulation of SRBD1 elevated p53 levels, thereby activating the p53 signaling pathway. As an RNA bind protein, SRBD1 could bind to the 5'-UTR of target genes and regulate RNA translation. We further conducted RNA immunoprecipitation using anti-SRDB1 antibody and noticed 29 hub RNA, including RPL11. RPL11 could inhibit MDM2-mediated p53 ubiquitination. SRBD1 upregulation promoted RPL11 binding to MDM2 via elevating RPL11 protein levels, which in turn activated the p53 signaling. Disrupting the p53 signaling blocked SRBD1-induced glioma suppression. In mouse xenograft model, SRBD1 ectopic expression was effective in reducing the total M2 tumor-associated macrophages (TAMs) density and suppressed glioma tumor growth. In summary, these data show that SRBD1 has a critical role in inhibition of glioma tumor growth and M2 macrophage polarization, and targeting RPL11-MDM2-p53 signaling may be an effective strategy to improve therapy and survival for glioma patients. - Source: PubMed
Publication date: 2024/09/11
Chen HongfuGao ShupingWang PengXie ManyiZhang HuiFan YuechaoNie ErLan Qing