SLC39A4

Last update 08 May 2025

Basic Info

Synonyms

acrodermatitis enteropathica, zinc-deficiency type, AEZ, AWMS2

+ [7]

Introduction

Selective transporter that mediates the uptake of Zn(2+) (PubMed:17202136, PubMed:22242765, PubMed:27321477, PubMed:28875161, PubMed:31164399, PubMed:31914589, PubMed:31979155, PubMed:33837739, PubMed:36473915). Plays an essential role for dietary zinc uptake from small intestine (By similarity). The Zn(2+) uniporter activity is regulated by zinc availability (PubMed:17202136, PubMed:32348750). Exhibits also polyspecific binding and transport of Cu(2+), Cd(2+) and possibly Ni(2+) but at higher concentrations (PubMed:22242765, PubMed:31914589).

100 Clinical Results associated with SLC39A4

100 Translational Medicine associated with SLC39A4

0 Patents (Medical) associated with SLC39A4

337

Literatures (Medical) associated with SLC39A4

01 Mar 2025·Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms

Transcriptional responses of three slc39a/zip members (zip4, zip5 and zip9) and their roles in Zn metabolism in grass carp (Ctenopharyngodon idella)

Article

Author: Liu, Tao ; Xu, Yi-Chuang ; Liu, Lu-Lu ; Xu, Peng-Cheng ; Luo, Zhi ; Guo, Jia-Cheng ; Zhang, Tian-Hua

In order to explore the regulatory mechanism of zip4, zip5 and zip9 in zinc metabolism of grass carp (Ctenopharyngodon idella), the effects of zinc (Zn) on the mRNA expression of zip4, zip5 and zip9 were investigated. Compared to the control, the mRNA levels of zip4 and zip9 were significantly reduced under low and high zinc in L8824 cells; the mRNA expression level of zip5 was significantly increased under low and high zinc incubation. Then, their promoter sequences were cloned, which were 2361 bp, 2004 bp and 2186 bp sequences for zip4, zip5 and zip9 promoters, respectively. The transcriptional activities of the three promoters had different responses to Zn treatment. The transcriptional factor signal transducer and activator of transcription 3 (STAT3) had specific binding sites at -1111/-1121 bp of zip5 promoter and at -1679/-1689 bp of zip9 promoter. Similarly, krüppel-like factor 4 (KLF4) could specifically bind to the -599/-609 bp sequence on the zip5 promoter and the -261/-272 bp sequence on the zip9 promoter. The results of electrophoretic mobility-shift assay (EMSA) and Chromatin immunoprecipitation (ChIP) indicated that Zn incubation increased DNA binding capacity of STAT3 to zip5 and zip9 promoters, and decreased DNA binding capacity of KLF4 to zip5 and zip9 promoters. This study provides a good basis for elucidating the regulatory mechanism of zinc metabolism in the vertebrates.

01 Mar 2025·Journal of Genetic Engineering and Biotechnology

Exploration of crucial stromal risk genes associated with prognostic significance and chemotherapeutic opportunities in invasive ductal breast carcinoma

Article

Author: Tang, Guohua ; Zhang, Yang ; Geng, Wei ; Yu, Yang ; Wang, Zhi

BACKGROUNDFew studies revealed that stromal genes regulate the tumor microenvironment (TME). However, identification of key-risk genes in the invasive ductal breast carcinoma-associated stroma (IDBCS) and their associations with the prediction of risk group remains lacking.METHODSThis study used the GSE9014, GSE10797, GSE8977, GSE33692, and TGGA BRCA datasets. We explored the differentially expressed transcriptional markers, hub genes, gene modules, and enriched KEGG pathways. We employed a variety of algorithms, such as the log-rank test, the LASSO-cox model, the univariate regression model, and the multivariate regression model, to predict prognostic-risk genes and the prognostic-risk model. Finally, we employed a molecular docking-based study to explore the interaction of sensitive drugs with prognostic-risk genes.RESULTSIn comparing IDBCS and normal stroma, we discovered 1472 upregulated genes and 1400 downregulated genes (combined ES > 0585 and adjusted p-value < 0.05). The hub genes enrich cancer, immunity, and cellular signaling pathways. We explored the 12 key risk genes (ADAM8, CD86, CSRP1, DCTN2, EPHA1, GALNT10, IGFBP6, MIA, MMP11, RBM22, SLC39A4, and SYT2) in the IDBCS to identify the high-risk group and low-risk group patients. The high-risk group had a lower survival rate, and the constructed ROC curves evaluated the validity of the risk model. Expression validation and diagnostic efficacy revealed that the key stromal risk genes are consistently deregulated in the high-risk group and high stromal samples of the TCGA BRCA cohort. The expression of crucial risk genes, including CD86, CSRP1, EPHA1, GALNT10, IGFBP6, MIA, and RBM22 are associated with drug resistance and drug sensitivity. Finally, a molecular docking study explored several sensitive drugs (such as QL-XII-61, THZ-2-49, AZ628, NG-25, lapatinib, dasatinib, SB590885, and dabrafenib) interacted with these essential risk genes through hydrogen bonds and other chemical interactions.CONCLUSIONSExploring essential prognostic-risk genes and their association with the prognosis, diagnostic efficacy, and risk-group prediction may provide substantial clues for targeting the breast cancer stromal key-risk genes.

27 Feb 2025·Nucleic Acids Research

Genetic dissection of MutL complexes in Arabidopsis meiosis

Article

Author: Pradillo, Mónica ; Santos, Juan L ; Kbiri, Nadia ; Sáez-Zárate, Esperanza ; Dluzewska, Julia ; Ziolkowski, Piotr A ; Pelé, Alexandre ; Dziegielewski, Wojciech ; Mata-Villanueva, Ana ; Fernández-Jiménez, Nadia

AbstractDuring meiosis, homologous chromosomes exchange genetic material through crossing over. The main crossover pathway relies on ZMM proteins, including ZIP4 and HEI10, and is typically resolved by the MLH1/MLH3 heterodimer, MutLγ. Our analysis shows that while MUS81 may partially compensate for MutLγ loss, its role remains uncertain. However, our multiple mutant analysis shows that MUS81 is unlikely to be the sole resolvase of ZMM-protected recombination intermediates when MutLγ is absent. Comparing genome-wide crossover maps of mlh1 mutants with ZMM-deficient mutants and lines with varying HEI10 levels reveals that crossover interference persists in mlh1 but is weakened. The significant crossover reduction in mlh1 also increases aneuploidy in offspring. The loss of MutLγ can be suppressed by eliminating the FANCM helicase. Combined with the lower-than-expected chiasma frequency, this suggests that in MutLγ absence, some ZMM-protected intermediates are ultimately resolved by DNA helicases and/or their complexes with Top3α. Elevated MLH1 or MLH3 expression moderately increases crossover frequency, while their misregulation drastically reduces crossover numbers and plant fertility, highlighting the importance for tight control of MLH1/MLH3 levels. By contrast, PMS1, a component of the MutLα endonuclease, appears uninvolved in crossing over. Together, these findings demonstrate the unique role of MutLγ in ZMM-dependent crossover regulation.

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SLC39A4

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