Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Iron (Fe) deficiency is counteracted by a suite of responses to ensure maintenance of vital processes for which Fe is essential. Here, we report on transcriptional changes upon Fe deficiency, investigated in two Arabidopsis (Arabidopsis thaliana) accessions, Columbia (Col-0) and C24. Functional modules of the Arabidopsis Fe deficiency syndrome were inferred from clustering of Fe-responsive genes according to their coexpression. It was found that the redistribution of transition metals is an integral part of the reduction-based response to Fe starvation. The differential expression of metal transporters under the control of the FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR appeared to reflect an anticipated reaction rather than a response to the actual change in metal distribution. In contrast, the regulation of the zinc transporters ZRT/IRT-LIKE PROTEIN2 (ZIP2), ZIP3, ZIP4, and ZIP9 was dependent on the cellular zinc level, and their regulation by Fe was a secondary effect. Cellular Fe homeostasis was found to be closely coupled to Fe-related processes in the plastids. Using clustered genes as bait in gene-fishing experiments, we were able to attribute potentially important roles for gene candidates that have no previously described function in the Fe deficiency response. These results demonstrate a conceptually novel and integrative view into the regulation and interactions that allow Arabidopsis to adapt to suboptimal Fe availability.
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PMID:Transcriptional profiling of the Arabidopsis iron deficiency response reveals conserved transition metal homeostasis networks. 2018 52

Rapid, cell surface-initiated, pregenomic androgen actions have been described in various vertebrate cells, but the receptors mediating these actions remain unidentified. We report here the cloning and expression of a cDNA from Atlantic croaker (Micropogonias undulatus) ovaries encoding a 33-kDa, seven-transmembrane protein with binding and signaling characteristics of a membrane androgen receptor that is unrelated to any previously described steroid receptor. Instead, croaker membrane androgen receptor has 81-93% amino acid sequence identity with zinc transporter ZIP9 (SLC39A9) subfamily members, indicating it is a ZIP9 protein. Croaker ZIP9 is expressed in gonadal tissues and in brain and is up-regulated in the ovary by reproductive hormones. Croaker ZIP9 protein is localized to plasma membranes of croaker granulosa cells and human breast cancer (SKBR-3) cells stably transfected with ZIP9. Recombinant croaker ZIP9 has a high affinity (dissociation constant, Kd, 12.7 nM), limited capacity (maximal binding capacity 2.8 nM/mg protein), displaceable, single binding site-specific for androgens, characteristic of steroid receptors. Testosterone activates a stimulatory G protein coupled to ZIP9, resulting in increased cAMP production. Testosterone promotes serum starvation-induced cell death and apoptosis in transfected cells and in croaker ovarian follicle cells that is associated with rapid increases in intracellular free zinc concentrations, suggesting an involvement of zinc in this nonclassical androgen action to promote apoptosis. These responses to testosterone are abrogated by treatment with ZIP9 small interfering RNA. The results provide the first evidence that zinc transporter proteins can function as specific steroid membrane receptors and indicate a previously unrecognized signaling pathway mediated by steroid receptors involving alterations in intracellular zinc.
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PMID:Identification and characterization of membrane androgen receptors in the ZIP9 zinc transporter subfamily: I. Discovery in female atlantic croaker and evidence ZIP9 mediates testosterone-induced apoptosis of ovarian follicle cells. 2532 26