Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain

In the paper

“Research indicates SGK1 plays a positive role in neuronal apoptosis during cerebral ischemia (Chaudhary et al., 2023; Zhang et al., 2014).”

What the sources say

• ?Not checked — no full text of the sourcecites Chaudhary et al., 2023 source
• Disputed

  The paper reports the opposite of a pro-apoptotic role: in its discussion of the cell experiments, SGK1 overexpression markedly reduced apoptosis after oxygen-glucose deprivation. Figure 6 also describes SGK1 transfection as protecting rats against ischemia/reperfusion-induced neuronal apoptosis. (LLM, conf=0.88)

  Checked by a reasoning model — may be wrong.

  cites Zhang et al., 2014 sourceExperimental — accuracy not yet measured

In the paper

“Studies suggest SGK1 enhances ENaC activity by increasing the expression of ENaC in the plasma membrane”

What the sources say

• Supported

  The Discussion states that sgk activates ENaC by increasing the number of channels in the plasma membrane. The experiments were performed in Xenopus oocytes, and the paper reports more surface channels rather than a change in channel open probability. (LLM, conf=0.94)

  cites Alvarez de la Rosa et al., 1999 source

In the paper

“Recent studies indicate the PI3K/AKT/SGK1 pathway aids in stimulating ENaC transport, pivotal in maintaining the integrity of the alveolar barrier”

What the sources say

• ?Not checked — no full text of the sourcecites Fei et al., 2021 source
• Partly supported

  The Discussion (page unavailable) reports that albumin activates PI3K/AKT/SGK1 signaling, increases ENaC-mediated Na+ transport, and improves barrier integrity; PI3K inhibition abolished the stimulatory effects. It does not establish the claim’s further link that ENaC transport itself is pivotal to maintaining alveolar barrier integrity. The Introduction describes ENaC transport as driving alveolar fluid clearance, while the Discussion treats barrier integrity as important for that clearance. (LLM, conf=0.84)

  cites Laube and Thome, 2022 sourceExperimental — accuracy not yet measured

In the paper

“SGK1 helps regulate cellular osmoregulation, primarily through the activation of key ion channels”

What the sources say

• Partly supported

  The Abstract and Discussion report that sgk increases sodium transport by increasing the number of epithelial sodium channels at the surface of Xenopus oocytes. They do not establish that SGK1 regulates cellular osmoregulation primarily through ion channels in general; the study examines one channel type and does not test that broader claim. (LLM, conf=0.86)

  cites Alvarez de la Rosa et al., 1999 sourceExperimental — accuracy not yet measured
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Lang et al., 2009a
• ?Not checked — no full text of the sourcecites Pongs, 2008 source

In the paper

“Knocking down p38 or SGK1 in macrophages using Adeno-Associated Virus (AAV) can reduce IL-4-induced M2 macrophage polarization in vitro”

What the sources say

• ?Could not verify

  The Results section on SGK-1 and autophagy reports SGK1 knockout in hepatocytes, not macrophages. Searches for p38, AAV, IL-4, and M2 polarization found no passage in our copy addressing the claimed macrophage experiment. (LLM, conf=0.78)

  cites Zhou et al., 2019 sourceExperimental — accuracy not yet measured

In the paper

“The p38/MAPK/SGK1 signaling pathway mediates many inflammatory responses in reaction to various stimuli”

What the sources say

• Partly supported

  The Introduction and section 2.3 describe p38 MAPK as important in inflammatory responses and activated by varied stimuli. The cited paper does not identify SGK1 as part of that signaling pathway, so it supports the p38/MAPK portion but not the full p38/MAPK/SGK1 claim. (LLM, conf=0.88)

  cites Yang et al., 2014 sourceExperimental — accuracy not yet measured

In the paper

“SGK1 is also known to activate a variety of ion channels, including sodium, calcium, potassium and chloride”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Lang et al., 2009b
• ?Not checked — no full text of the sourcecites Lang and Shumilina, 2013 source
• Supported

  The “SGK1-sensitive channels” section reports that SGK1 stimulates or up-regulates sodium channels (ENaC and SCN5A), potassium channels (ROMK1 and others), chloride channels (including ClC2 and CFTR), and calcium channels (including TRPV4–6). The supplied passages do not provide page numbers. (LLM, conf=0.94)

  cites Lang et al., 2014 source

In the paper

“SGK1 and its phosphorylated target NDRG1 are involved in the regulation and maturation of NF-κB signaling in antigen-presenting dendritic cells”

What the sources say

• Supported

  The Discussion reports that loss of SGK1 reduces NDRG1 phosphorylation and increases NF-κB nuclear localization in dendritic cells; NDRG1 silencing also increases nuclear NF-κB. It concludes that these effects influence dendritic-cell maturation. The supplied passages have section labels but no page numbers. (LLM, conf=0.92)

  cites Schmid et al., 2014 source

In the paper

“Interestingly, inhibiting the expression of SGK1 can induce the expression of Brain-Derived Neurotrophic Factor (BDNF) in T cells under Th17 differentiating conditions”

What the sources say

• Partly supported

  The Results section (Fig. 4B; page unavailable) reports that celastrol lowered SGK1 expression and raised BDNF expression in T cells cultured under Th17-differentiation conditions. It does not show that inhibiting SGK1 itself induced BDNF: the Results section on MAPK (Fig. 5; page unavailable) identifies p38 MAPK as an upstream regulator of both genes. (LLM, conf=0.87)

  cites Venkatesha and Moudgil, 2019 sourceExperimental — accuracy not yet measured

In the paper

“Gene silencing or chemical inhibition of p38/MAPK, NFAT5, or SGK1 can negate the development of Th17 cells induced by high salt environments”

What the sources say

• Supported

  The paper’s Abstract directly states that gene silencing or chemical inhibition of p38/MAPK, NFAT5 or SGK1 abrogates high-salt-induced Th17 cell development. The mechanistic passages also report reduced Th17 polarization or IL-17A production after inhibition or silencing. (LLM, conf=0.95)

  cites Kleinewietfeld et al., 2013 source

In the paper

“However, a more specific study has revealed that in the cerebral cortex of HD patients, SGK1 protein expression is downregulated”

What the sources say

• Partly supported

  The Results section on causal network modeling reports that Sgk1 is downregulated in R6/2 mice. The Results section on human HD validation reports decreased cortical protein levels for PRKCE, not SGK1. Thus, the cited paper supports SGK1 downregulation in a mouse model but not the claimed decrease in SGK1 protein in patients’ cerebral cortex. (LLM, conf=0.85)

  cites Lim et al., 2022 sourceExperimental — accuracy not yet measured

In the paper

“In the Tau transgenic mouse model, a prolonged high-fat diet activates SGK1, which promotes Tau pathology through the phosphorylation of Tau at the Ser214 site and the activation of an essential Tau kinase, GSK-3β”

What the sources say

• Supported

  The Results describe five months of high-fat diet in Tg601 tau-transgenic mice and report increased tau phosphorylation at Ser214 and signs of GSK-3β activation. The SGK1-mediated tau phosphorylation and GSK-3β activation Results section links SGK1 to both mechanisms and to tau aggregation. (LLM, conf=0.92)

  cites Elahi et al., 2021 source

In the paper

“In HD models, oligodendrocytes exhibit maturation and functional impairments (Wilton and Stevens, 2020), associated with changes in SGK1 expression, particularly in myelination and maintenance”

What the sources say

• Partly supported

  In “Mouse models of HD reveal deficits in oligodendrocyte biology and myelination” (page not provided), the review reports impaired myelin structure, gene expression, and remyelination in HD mice. It says impaired oligodendrocyte differentiation *could* explain early myelination deficits, but does not establish a maturation impairment. The Wilton and Stevens citation is attached to the clause before SGK1 expression, so that later association is not assessed here. (LLM, conf=0.85)

  cites Wilton and Stevens, 2020 sourceExperimental — accuracy not yet measured
• Partly supported

  The Results sections on R6/2 oligodendrocytes and causal network modeling report maturation and myelination-related impairments, and identify Sgk1 as downregulated in R6/2 mice. The Discussion describes a possible inability to turn over myelin components, but does not establish that SGK1 changes specifically impair myelination or myelin maintenance. The indexed passages have no page numbers. (LLM, conf=0.85)

  cites Lim et al., 2022 sourceExperimental — accuracy not yet measured

In the paper

“The SGK1-dependent phosphorylation of NDRG1 is a marker of mTORC2 activation”

What the sources say

• Supported

  The Results section states that mTORC2 activates SGK1, which then phosphorylates NDRG1, and reports measuring SGK1-dependent NDRG1 phosphorylation with a phospho-specific antibody. The Discussion also calls NDRG1 a distal effector of mTORC2 activation. Together, these passages support describing the phosphorylation as a marker of that activation; page numbers are unavailable in our copy. (LLM, conf=0.88)

  cites Cai et al., 2017 source

In the paper

“Additionally, the aging of glial cells can trigger degeneration of dopaminergic neurons, further leading to the onset and progression of PD”

What the sources say

• Partly supported

  The Results section reports that factors secreted by paraquat-induced senescent astrocytes reduced the viability of cultured dopaminergic neurons. It also reports that depleting senescent cells prevented a decline in a dopaminergic-neuron marker in paraquat-treated mice. These findings support a contribution to PD-related neuropathology, but do not establish that aging of glial cells generally triggers the onset or progression of human Parkinson’s disease (page numbers unavailable in our copy). (LLM, conf=0.88)

  cites Chinta et al., 2018 sourceExperimental — accuracy not yet measured

In the paper

“Multiple studies have shown that the downregulation of SGK1 can exacerbate the progression of PD through various mechanisms”

What the sources say

• ?Not checked — no full text of the sourcecites Heo et al., 2023 source
• Partly supported

  The Discussion links reduced SGK1 to several possible PD-related mechanisms, including loss of neuroprotection and increased intestinal α-synuclein. It says reduced SGK1 may imply accelerated deterioration, but does not demonstrate that downregulation exacerbates PD progression; it also reports that SGK1 inhibition in glia improved outcomes in an animal model. Page numbers were not provided in our copy. (LLM, conf=0.83)

  cites Seo et al., 2023 sourceExperimental — accuracy not yet measured
• Supported

  The Discussion (p. 6) says declining SGK1 may further exacerbate PD and discusses several possible pathways, including oxidative-stress-related cell death, glutamate effects, and increased α-synuclein expression. It also cites prior studies of SGK1’s protective role. The paper’s own experimental evidence comes from a Parkinsonism mouse model and SH-SY5Y cells, rather than direct measurement of progression in patients. (LLM, conf=0.86)

  cites Yeo et al., 2018 source

In the paper

“Detailed single-cell sequencing has also shown a downregulation of SGK1 protein expression in oligodendrocytes”

What the sources say

• Partly supported

  The Results section on causal network modeling reports that Sgk1 is downregulated in the oligodendrocyte/precursor-cell network of R6/2 Huntington disease mice. But single-nucleus RNA sequencing measures gene expression, not protein expression; the cited passage does not establish that SGK1 protein is reduced specifically in oligodendrocytes. (LLM, conf=0.88)

  cites Lim et al., 2022 sourceExperimental — accuracy not yet measured

In the paper

“A transient elevation in SGK1 levels within the brain may improve cell survival and neuroprotection following a stroke”

What the sources say

• Supported

  The Discussion states that transient augmentation of brain Sgk1 could be beneficial in stroke and other acute neurological states. Its tentative wording matches the claim’s “may”; the paper does not present this as a proven treatment effect. (LLM, conf=0.94)

  cites McCaig et al., 2019 source

In the paper

“After MCAO, inhibiting SGK1 in the lateral ventricles of rats within the thrombolytic treatment window reduced the percentage of cortical infarction and blood-brain barrier disruption”

What the sources say

• Supported

  Materials and methods (Animals) reports that the SGK1 inhibitor GSK650394 was injected into the left lateral ventricle of rats 10 minutes after MCAO. The Discussion reports a smaller infarct and less BBB disruption during the first few hours of ischemia-reperfusion, within the thrombolysis therapy time window; the Conclusions specifically identify a reduced cortical infarct. (LLM, conf=0.94)

  cites Chi et al., 2021 source

In the paper

“Overexpression of SGK1 partially restores the activation of Akt and GSK-3β, reducing hippocampal neuronal apoptosis in rats following OGD or MCAO via the PI3K/Akt/GSK-3β pathway”

What the sources say

• Partly supported

  The paper reports that SGK1 overexpression partially restored Akt and GSK-3β activation and reduced apoptosis in cultured rat hippocampal neurons after OGD, with PI3K/Akt signaling implicated. Its MCAO experiment also found reduced neuronal apoptosis after SGK1 transfection, but measured apoptotic cells in the ischemic penumbral cortex, not the hippocampus (Fig. 6; page unavailable). Thus the claim's hippocampal-neuron specificity is not supported for MCAO. (LLM, conf=0.88)

  cites Zhang et al., 2014 sourceExperimental — accuracy not yet measured

In the paper

“The role of SGK1 in metabolic pathways and glucose uptake may be disrupted and potentially exacerbate the pathological process of HD”

What the sources say

• Partly supported

  In Results, under causal network modeling, the paper says Sgk1 regulates transporters involved in metabolic pathways and glucose uptake and is downregulated in R6/2 mice, indicating a potential loss of function in HD. It does not establish that this loss exacerbates HD pathology. (LLM, conf=0.82)

  cites Lim et al., 2022 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites Mason et al., 2021 source

In the paper

“in clinical samples of DD, a significant negative correlation has been observed between the mRNA levels of SGK1 and BDNF”

What the sources say

• Supported

  The section “Increased SGK1 mRNA Expression in Depressed Patients” reports a negative correlation between SGK1 and BDNF mRNA levels in its clinical sample (r = -0.32, P = 0.05). The sample included patients with major depression. (LLM, conf=0.91)

  cites Anacker et al., 2013 source

In the paper

“during heart failure, the activation of SGK1 is associated with a reduction in dendritic spine density, potentially linked to TNF-α signaling pathways”

What the sources say

• Supported

  The Abstract (Methods and Results) states that increased SgK1 phosphorylation potentially plays a role in the heart-failure-associated reduction of dendritic spine density and may be TNF-α dependent. The Results section reports increased SgK1 phosphorylation in mice with heart failure and its reduction after TNF-α scavenging. The claim appropriately presents the link as potential rather than established. (LLM, conf=0.91)

  cites Meissner et al., 2015 source

In the paper

“After MCAO in rats, knockout of SGK1 upregulates the expression of beclin-1 and LC-3, aggravating dysregulated autophagy and neuronal apoptosis”

What the sources say

• Partly supported

  The Discussion reports that SGK1 knockdown upregulated beclin-1 and LC-3 in the rat MCAO model, and the apoptosis results report increased apoptosis. However, the experiments used shRNA knockdown, not knockout, and tested these effects in rats receiving intracarotid cold saline infusion. The claim omits that treatment condition and describes the autophagy effect more strongly than the measured marker changes establish. (LLM, conf=0.87)

  cites Wang et al., 2019 sourceExperimental — accuracy not yet measured

In the paper

“Abnormal GR activation contributes to neuronal apoptosis and degeneration by reducing the expression of BDNF and inhibiting cellular proliferation”

What the sources say

• Partly supported

  The Abstract reports that dexamethasone reduced BDNF mRNA in mouse neuronal cultures and that a GR antagonist abolished the effect. The Discussion suggests altered BDNF expression may affect neuronal structure and function, but the paper does not establish that GR activation causes neuronal apoptosis or degeneration, or that it inhibits cellular proliferation. (LLM, conf=0.88)

  cites Chen et al., 2017 sourceExperimental — accuracy not yet measured
• Partly supported

  The HPA-axis section (page unavailable) says high glucocorticoid levels mediated by GR can cause apoptosis in hippocampal neurons. The Glucocorticoids section (page unavailable) reports reduced hippocampal progenitor-cell proliferation and says high glucocorticoid doses inhibit production of brain-derived neurotrophic factor. It does not establish that reduced BDNF and proliferation cause neuronal apoptosis or degeneration, and it notes increased proliferation in a separate cortical stem-cell experiment. (LLM, conf=0.86)

  cites Kino, 2015 sourceExperimental — accuracy not yet measured
• Partly supported

  The ‘Glucocorticoid Effect on Neural Stem/Progenitor Cells’ section reports that increased glucocorticoids activate GR and reduce neural stem/progenitor-cell proliferation. It also reports reduced BDNF expression after stress or glucocorticoid exposure and GR-mediated repression of BDNF transcription. The paper does not establish that these effects cause neuronal apoptosis or degeneration. (LLM, conf=0.88)

  cites Odaka et al., 2017 sourceExperimental — accuracy not yet measured

In the paper

“the plasticity of white matter architecture and myelination is regulated by activity-dependent modulation of SGK1 expression in oligodendrocytes”

What the sources say

• Partly supported

  The Introduction (page not supplied) describes activity-dependent myelination and identifies SGK1 as a potential contributor to oligodendrocyte plasticity. The Discussion (page not supplied) says stress- and time-of-day regulation of Sgk1 expression may contribute to experience-dependent changes. Neither passage establishes that modulation of SGK1 expression regulates white matter architecture or myelination, as the claim states. (LLM, conf=0.88)

  cites Hinds et al., 2017 sourceExperimental — accuracy not yet measured

In the paper

“In the striatum of mice, a significant increase of approximately 1.5 to 2-fold in the transcriptional levels of SGK1 was observed following acute ketamine treatment”

What the sources say

• Supported

  The ‘Validation of ketamine-induced alterations in gene expression’ section reports approximately 1.5- to 2-fold upregulation of Sgk1 transcripts in the mouse striatum after acute ketamine administration. It also states that the treatment effect was significant in the qPCR analysis; mRNA levels were measured 2 hours after administration. (LLM, conf=0.94)

  cites Ficek et al., 2016 source
• Partly supported

  The Results (page unavailable) report that Sgk1 was upregulated in mouse striatum samples after ketamine treatment. They also report a statistically significant increase in striatal Sgk1 mRNA, but that result was from the rat validation experiment. Our copy does not give the claimed approximately 1.5- to 2-fold increase in mice. (LLM, conf=0.88)

  cites Qiao et al., 2019 sourceExperimental — accuracy not yet measured

In the paper

“SGK1 acts as a downstream effector in the GR signaling pathway”

What the sources say

• Supported

  The Results section calls SGK1 a downstream effector of glucocorticoid signaling. The Discussion further identifies sgk1 as a gene used to assess activity of the glucocorticoid receptor (GR) pathway. Page numbers are not provided in our copy. (LLM, conf=0.94)

  cites Wegman-Points et al., 2020 source

In the paper

“amplification SGK1 expression inhibits apoptosis in rat basilar artery smooth muscle cells through a mitochondrial-dependent intrinsic pathway within these cells”

What the sources say

• Supported

  The Discussion states that SGK1 overexpression inhibited apoptosis through the mitochondria-dependent intrinsic pathway in basilar artery smooth muscle cells. The experiments concerned H2O2-induced apoptosis. (LLM, conf=0.94)

  cites Chen et al., 2020 source

In the paper

“in rats exposed to unpredictable chronic mild stress and prenatal stress, as well as in patients with DD, there is a significant increase in the expression of SGK1 in the hippocampus”

What the sources say

• Partly supported

  The “Increased Hippocampal SGK1 Expression in Rodent Stress Models” section reports significant increases in hippocampal SGK1 mRNA after both unpredictable chronic mild stress and prenatal stress in rats. The paper reports increased SGK1 in the peripheral blood of drug-free depressed patients, not in their hippocampus; that location is unsupported for the patient group. (LLM, conf=0.93)

  cites Anacker et al., 2013 sourceExperimental — accuracy not yet measured

In the paper

“Transcription, catalytic activity, and phosphorylation of SGK1 are upregulated in the VTA through chronic cocaine or morphine treatment”

What the sources say

• Supported

  The Discussion states that VTA SGK1 mRNA, catalytic activity, and phosphorylation are upregulated by chronic cocaine and morphine treatment. The Introduction also identifies transcriptional upregulation in the VTA and increases in catalytic activity and phosphorylation after chronic treatment. Page numbers were not provided in our copy. (LLM, conf=0.94)

  cites Doyle et al., 2020 source

In the paper

“the Swiss ADME tool, predicts the SGK1 inhibitors GSK650394, EMD638683, and SI113 will be unlikely to cross the BBB to access the CNS”

What the sources say

• Supported

  In Results and discussion, under “BBB penetration prediction of SGK1 inhibitors,” the authors say they used SwissADME to predict BBB crossing and that GSK650394, EMD638683, and SI113 were predicted unable to reach the CNS. The citing sentence accurately presents this as a prediction, not a measured result. (LLM, conf=0.94)

  cites Maestro et al., 2023 source

In the paper

“SGK1 activation is a multi-step process involving initial phosphorylation at Ser422 by mTORC2 and subsequent phosphorylation at Thr256 by PDK1”

What the sources say

• Supported

  Figure 7 (page not specified) describes hydrophobic-motif phosphorylation of SGK1 via mTORC2 as the step that enables PDK1 to induce T-loop phosphorylation and activation. The accompanying figure labels identify the two sites as S422 and T256, respectively. (LLM, conf=0.91)

  cites Garcia-Martinez and Alessi, 2008 source
• ?Not checked — no full text of the sourcecites Pearce et al., 2010 source

In the paper

“Activation of SGK1 reduces the severity and mortality of seizures following the status epilepticus in an M-current-dependent manner”

What the sources say

• Supported

  The section ‘Reduced Seizure Severity in B6.Tg.sgk1 Mice Depends on M-Current Activation’ reports that blocking the M-current abolished the transgenic mice’s protection against kainic-acid-induced seizure severity and mortality. The Discussion likewise identifies M-current upregulation as the main mechanism of protection. The supplied passages do not provide page numbers. (LLM, conf=0.93)

  cites Armas-Capote et al., 2020 source

In the paper

“SGK1 mitigates the Nedd4–2-mediated internalization of Kv7.2/3 channels, thereby regulating M-current and neuronal excitability, through the phosphorylation of Nedd4–2”

What the sources say

• Partly supported

  The Introduction says SGK1.1 activation upregulates M-current via Nedd4-2 phosphorylation and reduces hippocampal neuronal excitability. The section on CA1 pyramidal neurons also reports increased Nedd4-2 phosphorylation and describes increased Kv7.2/7.3 surface expression through a Nedd4-2-related mechanism. It does not establish the more specific claim that SGK1 reduces Nedd4-2-mediated channel internalization. (LLM, conf=0.84)

  cites Armas-Capote et al., 2020 sourceExperimental — accuracy not yet measured
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Martin-Batista et al., 2021b
• ?Could not verify

  The Abstract reports that Nedd4-2 reduces Kv1.3 current density and that Grb10 relieves this suppression. Our copy does not address SGK1 phosphorylation of Nedd4-2, Kv7.2/3 internalization, or M-current; searches for SGK1 and Kv7.2/3 found no passage supporting that mechanism. (LLM, conf=0.75)

  cites Velez et al., 2016 sourceExperimental — accuracy not yet measured

In the paper

“inactivating VTA SGK1 catalytic activity with an inactive SGK1 mutant (K127Q) significantly reduces cocaine-conditioned place preference without altering cocaine-seeking behavior”

What the sources say

• Partly supported

  The Results report that VTA K127Q expression significantly reduced cocaine conditioned place preference. They also report no change in cocaine self-administration or motivation to obtain cocaine infusions in male mice. Those tests support the narrower finding, but not an unqualified claim about cocaine-seeking behavior generally. (LLM, conf=0.83)

  cites Doyle et al., 2021 sourceExperimental — accuracy not yet measured

In the paper

“SGK1 modulates excitability by regulating Kv7.2/3 channels”

What the sources say

• Supported

  The Introduction reports that the neuronal SGK1 isoform SGK1.1 increases Kv7.2/3 currents and that neurons with boosted SGK1.1 activity show reduced excitability. It concludes that SGK1.1 regulates neuronal excitability through M-current modulation. The claim is a broad paraphrase of that finding. (LLM, conf=0.90)

  cites Miranda et al., 2013 source

In the paper

“the research outcomes vary due to inconsistencies in the pathological models, intervention agents, and the timing of interventions, among other factors”

In the paper

“Itani et al. reports sequence differences within the glucocorticoid response element in the 5′-flanking region among humans, rats, and mice, which significantly affect the degree of SGK1 activation by glucocorticoids”

What the sources say

• ?Not checked — no full text of the sourcecites Itani et al., 2002 source

In the paper

“SGK1 modulate neuron excitability by regulating the K+ channel”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Lang et al., 2009a
• ?Not checked — no full text of the sourcecites Pongs, 2008 source

In the paper

“These studies suggest SGK1 is an emerging potential therapeutic target for neurological disorders.”

In the paper

“This sequential phosphorylation cascade is essential for the functional activation of SGK1 in cellular signaling pathways.”

In the paper

“Ultimately, SGK1 appears to have a dual role in immune regulation, which varies depending on physiological states.”

In the paper

“These findings suggest that SGK1 plays a crucial role in various molecular pathways involved in memory formation.”

In the paper

“Overexpression of SGK1 in ovariectomized mice reverses the reduction in synaptic protein expression, spine, and synapse density in the CA1 region”

What the sources say

• ?Not checked — no full text of the sourcecites Liu et al., 2022 source

In the paper

“However, SGK1 contributes to the inflammatory response induced by salt loading in microglia”

What the sources say

• ?Not checked — no full text of the sourcecites Inoue et al., 2020 source

In the paper

“In rats, inhibiting expression of SGK1 in the medial prefrontal cortex (mPFC) leads to impaired recognition memory under stress conditions”

What the sources say

• ?Not checked — no full text of the sourcecites Park et al., 2021 source

In the paper

“Interestingly, both hyperosmotic and hypoosmotic stimuli can induce the expression of the SGK1 gene in a cell-type-dependent manner”

What the sources say

• ?Not checked — no full text of the sourcecites Rozansky et al., 2002 source

In the paper

“In 10-month-old APP/PS1 mice, SGK1 expression is significantly reduced”

What the sources say

• ?Not checked — no full text of the sourcecites Lian et al., 2020 source

In the paper

“Further influencing neuronal activity and signaling, SGK1 enhances the non-inactivating potassium currents in neurons”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Martin-Batista et al., 2021b

In the paper

“The PI3K-Sgk1 pathway inhibits the ubiquitination activity of Nedd4–2, which, in turn, promotes the membrane expression of Kv7.1 and Kv1.5 channels”

What the sources say

• ?Not checked — no full text of the sourcecites Andersen et al., 2013 source

In the paper

“In the context of spatial memory in the water maze, SGK1 enhances learning and memory capabilities by phosphorylating transcription factors such as Serum Response Factor (SRF) and cAMP Response Element-Binding Protein 1 (CREB1)”

What the sources say

• ?Not checked — no full text of the sourcecites Tyan et al., 2008 source

In the paper

“Recent studies found SGK1 to play a significant role in immune cells”

What the sources say

• ?Not checked — no full text of the sourcecites Inoue et al., 2020 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Inoue et al., 2016b

In the paper

“Also, inhibition of SGK1 enhances the inflammatory response in microglia via the NF-κB signaling pathway”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Inoue et al., 2016b

In the paper

“These findings indicate the increased rate of myelin regeneration observed in AD may be mediated by the SGK1/NDRG1.”

In the paper

“The increase in SGK1 expression levels in 3NP-treated mouse models may represent an adaptive response to mitochondrial dysfunction and cellular stress.”

In the paper

“The increased levels of SGK1 lead to a significant rise in hippocampal ADAM10 (α-secretase) and IDE (Aβ-degrading enzyme)”

What the sources say

• ?Not checked — no full text of the sourcecites Lian et al., 2020 source

In the paper

“These studies demonstrate that SGK1 plays a dual role in AD, with its effects varying depending on different pathways”

In the paper

“early PCR-based gene expression profiling methods, such as the Digital Expression Pattern Display, have identified that in the brains of MPTP-induced PD mice, increased SGK1 transcriptome levels coincide with the onset of dopaminergic cell death”

What the sources say

• ?Not checked — no full text of the sourcecites Stichel et al., 2005 source

In the paper

“In summary, the protective role of SGK1 in TBI is multi-targeted.”

In the paper

“Under prolonged exposure to negative environmental stressors, high concentrations of glucocorticoids produced along the HPA axis led to the overactivation of glucocorticoid receptors (GR) in central nervous system target cells”

What the sources say

• ?Not checked — no full text of the sourcecites Gray et al., 2017 source

In the paper

“These studies indicate the involvement of multiple neuroprotective mechanisms of SGK1 in HD.”

In the paper

“inactivation of SGK1 in Schwann cells shifts cell fate from proliferation to differentiation, promoting axonal and glial regeneration during peripheral nerve injury”

What the sources say

• ?Not checked — no full text of the sourcecites Okura et al., 2022 source

In the paper

“However, SGK1 exhibits contrasting effects in different models or observational indices following cerebral ischemia.”

In the paper

“Dietary restriction leads to a more pronounced increase in SGK1 gene expression, creating a closer association between SGK1 expression and phosphorylated GR in rats on a restricted diet compared to those with ad libitum feeding”

What the sources say

• ?Not checked — no full text of the sourcecites Perovic et al., 2022 source

In the paper

“In rats, six minutes of asphyxial CA causing global cerebral ischemia resulted in elevated SGK1 protein and mRNA in the hippocampus for the first three days post-CA, with a subsequent decline in mRNA by seventh day”

What the sources say

• ?Not checked — no full text of the sourcecites Lee et al., 2020 source

In the paper

“These suggest that SGK1 mediates the adverse outcomes in fetuses resulting from maternal drug addiction.”

In the paper

“GSK650394 inhibits the kinase activity of SGK1 by binding to its ATP-binding site, meaning it competes with the natural substrate ATP for the same binding site”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites He et al., 2022

In the paper

“suggesting that increased SGK1 may represent a benign compensatory phenomenon in epilepsy.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Lu et al., 2010

In the paper

“SGK1 expression in brain regions and cell types also exhibits region-specific characteristics”

What the sources say

• ?Not checked — no full text of the sourcecites Iwata et al., 2004 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Wu et al., 2024