|
Hyperinsulinism
|
0.010 |
Biomarker
|
disease |
BEFREE |
Zip14 knockout mice display hyperinsulinemia and impaired insulin secretion in high glucose conditions.
|
31197210 |
2019 |
|
nervous system disorder
|
0.010 |
Biomarker
|
group |
BEFREE |
Bi-allelic mutations in any of these transporter proteins disrupt the manganese equilibrium and lead to neurological disease: Hypermanganesaemia with dystonia 1 (SLC30A10 deficiency) and hypermanganesaemia with dystonia 2 (SLC39A14 deficiency) are characterised by manganese neurotoxicity while SLC39A8 mutations cause a congenital disorder of glycosylation type IIn due to Mn deficiency.
|
31089831 |
2019 |
|
Laryngeal Squamous Cell Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
They and their ceRNA axis genes (particularly TMEM51-AS1-miR-106b-TRAPPC10; RUSC1-AS1-miR-16-SLC39A14) may be potentially important prognostic biomarkers for LSCC.
|
31565549 |
2019 |
|
Impaired insulin secretion
|
0.010 |
Biomarker
|
disease |
BEFREE |
Zip14 knockout mice display hyperinsulinemia and impaired insulin secretion in high glucose conditions.
|
31197210 |
2019 |
|
Cancer cachexia
|
0.010 |
Biomarker
|
disease |
BEFREE |
The potential of anti-ZIP14 antibodies and zinc chelation as anti-cachexia therapy should be tested in patients with cancer cachexia.
|
30920774 |
2019 |
|
CONGENITAL DISORDER OF GLYCOSYLATION, TYPE IIn
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Bi-allelic mutations in any of these transporter proteins disrupt the manganese equilibrium and lead to neurological disease: Hypermanganesaemia with dystonia 1 (SLC30A10 deficiency) and hypermanganesaemia with dystonia 2 (SLC39A14 deficiency) are characterised by manganese neurotoxicity while SLC39A8 mutations cause a congenital disorder of glycosylation type IIn due to Mn deficiency.
|
31089831 |
2019 |
|
Bone Diseases
|
0.010 |
Biomarker
|
group |
BEFREE |
Collectively, we reveal ZIP14 as a novel regulator of bone homeostasis, and that manipulating ZIP14 might be a therapeutic strategy for bone diseases.
|
29621230 |
2018 |
|
Cachexia
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
Metastatic cancers promote cachexia through ZIP14 upregulation in skeletal muscle.
|
29875463 |
2018 |
|
Heart failure
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
The expressions of ZIP14 and ZnT8 were significantly increased with decreased ZIP8 level in HF.
|
29333637 |
2018 |
|
Congestive heart failure
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
The expressions of ZIP14 and ZnT8 were significantly increased with decreased ZIP8 level in HF.
|
29333637 |
2018 |
|
Hyperostosis
|
0.010 |
Biomarker
|
disease |
BEFREE |
Conditional mouse models support the role of SLC39A14 (ZIP14) in Hyperostosis Cranialis Interna and in bone homeostasis.
|
29621230 |
2018 |
|
Neoplasm Metastasis
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
ZIP14 is upregulated in cachectic muscles of mice and in patients with metastatic cancer and can be induced by TNF-α and TGF-β cytokines.
|
29875463 |
2018 |
|
Neoplasms
|
0.010 |
AlteredExpression
|
group |
BEFREE |
Expression levels in tumor tissue and survival time revealed a negative correlation for ZIP4 and ZIP14, and in part for ZnT9 (nuclear staining) (p < 0.05), whereas cytoplasmic staining of ZnT9 did not correlate with survival.
|
29895370 |
2018 |
|
Iron Overload
|
0.010 |
Biomarker
|
disease |
BEFREE |
Studies of <i>Slc39a14</i> knockout (<i>Slc39a14</i><sup>-/-</sup>) mice have documented that SLC39A14 is required for systemic growth, hepatic zinc uptake during inflammation, and iron loading of the liver in iron overload.
|
29437953 |
2018 |
|
Disseminated Malignant Neoplasm
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
ZIP14 is upregulated in cachectic muscles of mice and in patients with metastatic cancer and can be induced by TNF-α and TGF-β cytokines.
|
29875463 |
2018 |
|
Neurodegenerative Disorders
|
0.010 |
GeneticVariation
|
group |
BEFREE |
Homozygous exonic mutations in the manganese transporter SLC39A14 have recently been associated with a pediatric-onset neurodegenerative disorder characterized by brain manganese accumulation and clinical signs of manganese neurotoxicity, including parkinsonism-dystonia.
|
29685658 |
2018 |
|
Chronic Kidney Diseases
|
0.010 |
Biomarker
|
group |
BEFREE |
In CKD, iron deposition associated with increased intensity of iron importers (ZIP14, ZIP8), storage proteins (L-, H-ferritin), and/or decreased ferroportin abundance.
|
29921869 |
2018 |
|
Acute dystonia
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
We aimed to explore further biomarkers of Mn deposition in the central nervous system in two siblings presenting with acute dystonia and hypermanganesemia due to mutations in SLC39A14.
|
29382362 |
2018 |
|
HEMANGIOMA, CAPILLARY INFANTILE
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Conditional knock-in mice overexpressing L438R Zip14 in osteoblasts have a severe skeletal phenotype marked by a drastic increase in cortical thickness due to an enhanced endosteal bone formation, resembling the underlying pathology in HCI patients.
|
29621230 |
2018 |
|
Secondary Neoplasm
|
0.010 |
AlteredExpression
|
group |
BEFREE |
ZIP14 is upregulated in cachectic muscles of mice and in patients with metastatic cancer and can be induced by TNF-α and TGF-β cytokines.
|
29875463 |
2018 |
|
Hepatolenticular Degeneration
|
0.010 |
Biomarker
|
disease |
BEFREE |
This update will address: i) the manganese/zinc transporters (because two new treatable disorders were described in 2016 - SLC39A8 deficiency and SLC39A14 deficiency); ii) copper transporter disorders because we need to improve the treatment of patients with neurological symptoms due to Wilson's disease; and iii) iron homeostasis because recent progress in research into the metabolism of iron and its regulation helps us better understand several inborn errors affecting these pathways.
|
28303424 |
2017 |
|
Hypothyroidism
|
0.010 |
Biomarker
|
disease |
BEFREE |
To determine the mechanisms of manganese-induced hypothyroidism and understand how SLC30A10 and SLC39A14 cooperatively mediate manganese detoxification, here we produced <i>Slc39a14</i> single and <i>Slc30a10/Slc39a14</i> double knockout mice and compared their phenotypes with that of <i>Slc30a10</i> single knockouts.
|
28860195 |
2017 |
|
Neurologic Symptoms
|
0.010 |
Biomarker
|
group |
BEFREE |
This update will address: i) the manganese/zinc transporters (because two new treatable disorders were described in 2016 - SLC39A8 deficiency and SLC39A14 deficiency); ii) copper transporter disorders because we need to improve the treatment of patients with neurological symptoms due to Wilson's disease; and iii) iron homeostasis because recent progress in research into the metabolism of iron and its regulation helps us better understand several inborn errors affecting these pathways.
|
28303424 |
2017 |
|
Steatohepatitis
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
We propose ZIP14 mediates zinc transport into hepatocytes to inhibit protein-tyrosine phosphatase 1B (PTP1B) activity, which acts to suppress apoptosis and steatosis associated with hepatic ER stress.
|
28673968 |
2017 |
|
Hypoglycemia
|
0.010 |
Biomarker
|
disease |
BEFREE |
The Zip14 KO mice exhibited decreased circulating IL-6 with increased hepatic SOCS-3 following LPS, suggesting SOCS-3 inhibited insulin signaling which produced the hypoglycemia in this genotype.
|
23110240 |
2012 |