SLC11A1 (Human) Recombinant Protein (Q01)
- Known as:
- SLC11A1 (Human) Recombinant Protein (Q01)
- Catalog number:
- H00006556-Q01-25
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- SLC11A1 (Human) Recombinant Protein (Q01)
Related genes to: SLC11A1 (Human) Recombinant Protein (Q01)
- Gene:
- SLC11A1 NIH gene
- Name:
- solute carrier family 11 member 1
- Previous symbol:
- LSH, NRAMP, NRAMP1
- Synonyms:
- -
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-21
- Date modifiied:
- 2016-02-17
Related products to: SLC11A1 (Human) Recombinant Protein (Q01)
Related articles to: SLC11A1 (Human) Recombinant Protein (Q01)
- SLC11A1 is a key gene involved in the regulation of innate immunity, and its expression level is closely associated with disease resistance in livestock and poultry, making it an important candidate gene for disease-resistant breeding. The functional characteristics of the promoter region are central to deciphering the transcriptional regulatory mechanisms of a gene. In this study, we focused on the chicken SLC11A1 gene and retrieved sequences flanking the transcription start site (TSS) from the NCBI database. By integrating bioinformatic analysis with a dual-luciferase reporter assay system, we systematically identified the core promoter region and functionally characterized the regulatory roles of cis-regulatory element and their associated transcription factor binding profiles. Results revealed a canonical TATA-box element located at -31 bp to -28 bp upstream of the TSS of the chicken SLC11A1 gene. Functional analysis using a series of truncated luciferase reporter constructs demonstrated that the region from -172 bp to +19 bp constitutes the core promoter of the chicken SLC11A1 gene, with the segment from -172 bp to -36 bp being essential for basal transcriptional activity, the TATA-box was shown to synergistically enhance transcriptional efficiency when combined with this region. Prediction of transcription factor binding sites indicated that Sp1 exhibited the highest binding frequency within the core promoter, followed by C/EBPalpha and other factors. These findings define the fundamental regulatory architecture of the chicken SLC11A1 promoter, providing essential insights for future studies on the transcriptional regulation and biological functions of SLC11A1. - Source: PubMed
Publication date: 2026/07/02
Wang MengjieWang JingjingWang XiaoyaZhang LijieLiu XinranGao QianmeiLi QingheZhao Guiping - Tuberculosis (TB) remains a major infectious disease burden, and inter-individual heterogeneity in progression from exposure to active disease suggests contributions from host genetic factors. SLC11A1 (formerly NRAMP1) encodes a phagosomal divalent cation transporter implicated in macrophage-mediated antimicrobial defense; the non-synonymous rs17235409 polymorphism (D543N) has been evaluated in multiple populations with inconsistent results. We conducted a retrospective matched case-control study in Qiandongnan, Guizhou Province, China, including 50 patients diagnosed with TB (2022-2023) and 50 healthy controls frequency-matched by ethnicity and selected demographics. Participants were drawn from Miao, Dong, and other minority groups. Among TB cases, the frequencies of the GG, GA, and AA genotypes were 80.0%, 20.0%, and 0%, respectively, compared with 74.0%, 18.0%, and 8.0% among controls. The overall genotype distribution did not differ significantly between the 2 groups (P = .124). Under the dominant model, no significant association was observed between rs17235409 and TB susceptibility (OR = 0.71, 95% CI: 0.28-1.82; P = .635). Allelic analysis showed that the frequency of the A allele was lower in cases than in controls (10.0% vs 17.0%), but this difference was not statistically significant (OR = 0.54, 95% CI: 0.24-1.25; P = .214). Ethnicity-stratified analyses similarly showed no statistically detectable associations in Miao, Dong, or other groups. The minor allele frequency was 0.095, lower than the Han Chinese reference from 1000 Genomes. In this pilot study of multi-ethnic populations from southwestern China, no statistically significant association was identified between the SLC11A1 rs17235409 polymorphism and tuberculosis susceptibility. Although the A allele appeared less frequent among cases, the limited sample size and statistical power preclude definitive conclusions regarding modest or ethnic-specific effects. These findings provide preliminary genetic data from underrepresented ethnic minority populations and warrant validation in larger multicenter studies. - Source: PubMed
Chen ChaoGu DianjuXie Yunmi - Intra-abdominal infection frequently progresses to sepsis, where the liver is an early and commonly injured organ. In a cecal ligation and puncture (CLP) mouse model combined with bulk and single‑cell RNA sequencings, we observed marked neutrophil infiltration in the liver that correlated with injury severity. Sepsis‑associated neutrophils displayed a pro‑inflammatory phenotype and specifically upregulated the divalent metal transporter solute carrier family 11 member 1 (SLC11A1). Conditional knockout of Slc11a1 in neutrophils (Ly6G-Cre Slc11a1) significantly alleviated liver injury and improved survival. Mechanistically, SLC11A1 drives intracellular Fe accumulation and reactive oxygen species production via the Fenton reaction, promoting the formation of neutrophil extracellular traps (NETs). Hepatocytes were found to secrete C-X-C motif chemokine ligand 10 (CXCL10) through nuclear factor kappa B (NF‑κB) activation, which both recruit neutrophils and stimulates the JAK/STAT1/SLC11A1 axis, thereby enhancing NETs‑mediated pro‑inflammatory macrophage polarization. Clinically, peripheral blood CXCL10 levels correlated with liver injury markers in sepsis patients. Neutralization of CXCL10 using an anti-CXCL10 antibody or liver-specific knockdown of CXCL10 via Adeno-Associated Virus (AAV) reduced NETs formation and attenuated liver damage in CLP mice. This study delineates a "CXCL10-SLC11A1-NETs" signaling axis that exacerbates sepsis‑induced liver injury, offering a novel target for therapeutic intervention. - Source: PubMed
Publication date: 2026/07/13
Lin HaipingZheng ShicongSong PeiChang JieChen ZeweiLi CangYu MinWang LudeYu Shian - Myocardial ischemia-reperfusion (MIR) injury remains the leading cause of adverse outcomes after myocardial infarction, and its prevention remains a major therapeutic challenge. - Source: PubMed
Publication date: 2026/06/19
Dong YilinYang HaomingYang FanMeng Liang - Ferroptosis is a critical contributor to cardiomyocyte injury in acute myocardial infarction (AMI). This study aimed to identify key ferroptosis-associated genes and elucidate their roles in AMI. Transcriptomic datasets from AMI patients and healthy controls were analyzed to identify differentially expressed genes (DEGs). The role of the solute carrier family 11 member 1 (SLC11A1) was validated in vitro using a hypoxia/reoxygenation (H/R) model in H9c2 cardiomyocytes and in vivo using a murine AMI model. SLC11A1 expression was elevated in H/R-treated cardiomyocytes and infarcted murine hearts. SLC11A1 silencing reduced infarct size and improved cardiac function, and suppressed ferroptosis. Mechanistically, SLC11A1 led to the transcriptional suppression of glutathione peroxidase 4 (GPX4) mediated by the transcription factor specificity protein 1 (Sp1). This study identifies the SLC11A1-Sp1-GPX4 axis as a pivotal transcriptional regulator pathway driving ferroptosis in AMI. These findings highlight SLC11A1 as a promising therapeutic target in AMI. - Source: PubMed
Publication date: 2026/06/03
Zhang ShirongWang YeshuFeng YangmeiWang FangZhu Jiaqing