LIMK1 promotes the development of cervical cancer by up-regulating the ROS/Src-FAK/cofilin signaling pathway.

OBJECTIVE: In this study, we investigated the mechanism of action of LIMK1 in cervical cancer progression. METHODS: The biological role of LIMK1 in regulating the growth, invasion, and metastasis of cervical cancer was studied in SiHa, CaSki cells and nude mice tumor models. The role of LIMK1 in the growth of cervical cancer was evaluated by HE staining. The role of LIMK1 in the invasion, metastasis, and proliferation of cervical cancer was evaluated by cell scratch, Transwell, and monoclonal experiments. The interaction among LIMK1, ROS, and Src was evaluated by Western blotting. The effects of regulating ROS and p-Src expression on LIMK1 in the migration/invasion and proliferation of cervical cancer cells were evaluated through cellular functional assays. RESULTS: Overexpression of LIMK1 promoted tumor growth in nude mice. Cell scratch, Transwell, and monoclonal experiments suggested that LIMK1 promoted the invasion, metastasis, and proliferation of cervical cancer cells. Western blotting suggested that LIMK1 can promote the expression of ROS-related proteins NOX2, NOX4, p-Src, and downstream proteins p-FAK, p-ROCK1/2, p-Cofilin-1, F-actin and inhibit the expression of p-SHP2 protein. Correction experiments showed that LIMK1 regulated the expression of p-FAK and p-Cofilin-1 proteins by regulating ROS and p-Src. Through the detection of cervical cancer cell functions, it was found that the activation of ROS and p-Src induced by LIMK1 is an early event that promotes the migration, proliferation, and invasion of cervical cancer cells. CONCLUSIONS: LIMK1 promotes the expression of F-actin and promotes the development of cervical cancer by regulating the oxidative stress/Src-mediated p-FAK/p-ROCK1/2/p-Cofilin-1 pathway.

Inhibiting NF-κB inducing kinase improved the motor performance of ALS animal model.

BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a typical neurodegenerative disorder typically characterized by inflammation activation. However, the relationship between non-canonical NF-κB (ncNF-κB) pathway activation and ALS progression is not clear. METHODS: We tested the ncNF-κB pathway in the ALS animal model including hSOD1-G93A transgenic mice and TBK1 deletion mice.We treated age-matched SOD1-G93A mice with B022 (a NIK inhibitor) to investigate the role of NIK in the ALS animal model. We also established a new mice model by crossing SOD1-G93A mice with NIK+/- mice to further evaluate the interrelationship between the NIK and the disease progression in ALS animal model. RESULTS: In this study, we found the ncNF-κB pathway was activated in SOD1-G93A animal model and TBK1 deletion model. Inhibition of NIK activity by small molecule B022 significantly improved the motor performance of the ALS animal model. However, NIK deletion enhanced the mutant SOD1 toxicity by inflammatory infiltration. CONCLUSION: BK1 deletion and mutant SOD1 shared the common pathological feature possibly via effects on NIK activation and inhibitor of NIK could be a novel strategy for treating ALS.

Dynamic tracking of onion-like carbon nanoparticles in cancer cells using limited-angle holographic tomography with self-supervised learning.

This research presents a novel approach for the dynamic monitoring of onion-like carbon nanoparticles inside colorectal cancer cells. Onion-like carbon nanoparticles are widely used in photothermal cancer therapy, and precise 3D tracking of their distribution is crucial. We proposed a limited-angle digital holographic tomography technique with unsupervised learning to achieve rapid and accurate monitoring. A key innovation is our internal learning neural network. This network addresses the information limitations of limited-angle measurements by directly mapping coordinates to measured data and reconstructing phase information at unmeasured angles without external training data. We validated the network using standard SiO2 microspheres. Subsequently, we reconstructed the 3D refractive index of onion-like carbon nanoparticles within cancer cells at various time points. Morphological parameters of the nanoparticles were quantitatively analyzed to understand their temporal evolution, offering initial insights into the underlying mechanisms. This methodology provides a new perspective for efficiently tracking nanoparticles within cancer cells.

Field-Free Manipulation of Two-Dimensional Ferromagnet CrTe2 by Spin-Orbit Torques.

Electrical manipulation of magnetic states in two-dimensional ferromagnetic systems is crucial in information storage and low-dimensional spintronics. Spin-orbit torque presents a rapid and energy-efficient method for electrical control of the magnetization. In this letter, we demonstrate a wafer-scale spin-orbit torque switching of two-dimensional ferromagnetic states. Using molecular beam epitaxy, we fabricate two-dimensional heterostructures composed of low crystal-symmetry WTe2 and ferromagnet CrTe2 with perpendicular anisotropy. By utilizing out-of-plane spins generated from WTe2, we achieve field-free switching of the CrTe2 perpendicular magnetization. The threshold switching current density in CrTe2/WTe2 is 1.2 × 106 A/cm2, 20 times smaller than that of the CrTe2/Pt control sample even with an external magnetic field. In addition, the switching behavior can be modulated by external magnetic fields and crystal symmetry. Our findings demonstrate a controllable and all-electric manipulation of perpendicular magnetization in a two-dimensional ferromagnet, representing a significant advancement toward the practical implementation of low-dimensional spintronic devices.

Spin-orbit torque manipulation of sub-terahertz magnons in antiferromagnetic α-Fe2O3.

The ability to electrically manipulate antiferromagnetic magnons, essential for extending the operating speed of spintronic devices into the terahertz regime, remains a major challenge. This is because antiferromagnetic magnetism is challenging to perturb using traditional methods such as magnetic fields. Recent developments in spin-orbit torques have opened a possibility of accessing antiferromagnetic magnetic order parameters and controlling terahertz magnons, which has not been experimentally realised yet. Here, we demonstrate the electrical manipulation of sub-terahertz magnons in the α-Fe2O3/Pt antiferromagnetic heterostructure. By applying the spin-orbit torques in the heterostructure, we can modify the magnon dispersion and decrease the magnon frequency in α-Fe2O3, as detected by time-resolved magneto-optical techniques. We have found that optimal tuning occurs when the Néel vector is perpendicular to the injected spin polarisation. Our results represent a significant step towards the development of electrically tunable terahertz spintronic devices.

Above-room-temperature chiral skyrmion lattice and Dzyaloshinskii-Moriya interaction in a van der Waals ferromagnet Fe3-xGaTe2.

Skyrmions in existing 2D van der Waals (vdW) materials have primarily been limited to cryogenic temperatures, and the underlying physical mechanism of the Dzyaloshinskii-Moriya interaction (DMI), a crucial ingredient for stabilizing chiral skyrmions, remains inadequately explored. Here, we report the observation of Néel-type skyrmions in a vdW ferromagnet Fe3-xGaTe2 above room temperature. Contrary to previous assumptions of centrosymmetry in Fe3-xGaTe2, the atomic-resolution scanning transmission electron microscopy reveals that the off-centered FeΙΙ atoms break the spatial inversion symmetry, rendering it a polar metal. First-principles calculations further elucidate that the DMI primarily stems from the Te sublayers through the Fert-Lévy mechanism. Remarkably, the chiral skyrmion lattice in Fe3-xGaTe2 can persist up to 330 K at zero magnetic field, demonstrating superior thermal stability compared to other known skyrmion vdW magnets. This work provides valuable insights into skyrmionics and presents promising prospects for 2D material-based skyrmion devices operating beyond room temperature.

Study on Gamma sensory flicker for Insomnia.

OBJECTIVES: Insomnia has been the subject of much systematic research because it is a risk factor for a variety of diseases. There is some evidence that gamma sensory stimulation therapy has also been demonstrated to improve sleep quality for people with Alzheimer's disease. However, it is unclear whether this method is effective for treating insomnia. The principal objective of this project was to investigate the efficacy and safety of gamma sensory flicker in improving the sleep quality of insomnia patients. METHODS: Thirty-seven participants with insomnia were recruited for this prospective observational study. For a duration of 8 weeks, participants were exposed to flicker stimulation through a light and sound device. RESULTS: During the main phase of the study, adherence rates averaged 92.21%. Additionally, no severe adverse events were reported for flicker treatment. Analysis of sleep diaries indicated that 40 Hz flickers can enhance sleep quality by reducing sleep onset latencies, and arousals, and increasing total sleep duration. CONCLUSIONS: Gamma sensory flicker improves sleep quality in people suffering from insomnia.

A rare germline BMP15 missense mutation causes hereditary ovarian immature teratoma in human.

Ovarian immature teratomas (OITs) are malignant tumors originating from the ovarian germ cells that mainly occur during the first 30 y of a female's life. Early age of onset strongly suggests the presence of susceptibility gene mutations for the disease yet to be discovered. Whole exon sequencing was used to screen pathogenic mutations from pedigrees with OITs. A rare missense germline mutation (C262T) in the first exon of the BMP15 gene was identified. In silico calculation suggested that the mutation could impair the formation of mature peptides. In vitro experiments on cell lines confirmed that the mutation caused an 84.7% reduction in the secretion of mature BMP15. Clinical samples from OIT patients also showed a similar pattern of decrease in the BMP15 expression. In the transgenic mouse model, the spontaneous parthenogenetic activation significantly increased in oocytes carrying the T allele. Remarkably, a mouse carrying the T allele developed the phenotype of OIT. Oocyte-specific RNA sequencing revealed that abnormal activation of the H-Ras/MAPK pathway might contribute to the development of OIT. BMP15 was identified as a pathogenic gene for OIT which improved our understanding of the etiology of OIT and provided a potential biomarker for genetic screening of this disorder.

Phase separation of SHP2E76K promotes malignant transformation of mesenchymal stem cells by activating mitochondrial complexes.

Mesenchymal stem cells (MSCs), suffering from diverse gene hits, undergo malignant transformation and aberrant osteochondral differentiation. Src homology region 2-containing protein tyrosine phosphatase 2 (SHP2), a nonreceptor protein tyrosine phosphatase, regulates multicellular differentiation, proliferation, and transformation. However, the role of SHP2 in MSC fate determination remains unclear. Here, we showed that MSCs bearing the activating SHP2E76K mutation underwent malignant transformation into sarcoma stem-like cells. We revealed that the SHP2E76K mutation in mouse MSCs led to hyperactive mitochondrial metabolism by activating mitochondrial complexes I and III. Inhibition of complexes I and III prevented hyperactive mitochondrial metabolism and malignant transformation of SHP2E76K MSCs. Mechanistically, we verified that SHP2 underwent liquid-liquid phase separation (LLPS) in SHP2E76K MSCs. SHP2 LLPS led to its dissociation from complexes I and III, causing their hyperactivation. Blockade of SHP2 LLPS by LLPS-defective mutations or allosteric inhibitors suppressed complex I and III hyperactivation as well as malignant transformation of SHP2E76K MSCs. These findings reveal that complex I and III hyperactivation driven by SHP2 LLPS promotes malignant transformation of SHP2E76K MSCs and suggest that inhibition of SHP2 LLPS could be a potential therapeutic target for the treatment of activated SHP2-associated cancers.

Balancing the Ion/Electron Transport of Graphite Anodes by a La-Doped TiNb2O7 Functional Coating for Fast-Charging Li-Ion Batteries.

A functional coating layer (FCL) is widely applied in fast-charging lithium-ion batteries to improve the sluggish Li+ transport kinetics of traditional graphite anodes. However, blindly increasing the Li+ conductivity for FCL reduces the overall electron conductivity of the anodes. Herein, we decoupled the effect of La-doping on TiNb2O7 (TNO) in terms of the phase evolution, Li+/electron transport, and lithiation behavior, and then proposed a promising La0.1TNO FCL with balanced Li+/electron transport for a fast-charging graphite anode. By optimizing the doping concentration of La, more holes are introduced into the TNO as electron carriers without causing lattice distortion, thus maintaining the fast Li+ diffusion channel in TNO. As a result, the graphite with La0.1TNO FCL delivers an excellent capacity of 220.2 mAh g-1 (96.3% retention) after 450 cycles at 3 C, nearly twice that of the unmodified one.

Field-free switching of perpendicular magnetization by two-dimensional PtTe2/WTe2 van der Waals heterostructures with high spin Hall conductivity.

The key challenge of spin-orbit torque applications lies in exploring an excellent spin source capable of generating out-of-plane spins while exhibiting high spin Hall conductivity. Here we combine PtTe2 for high spin conductivity and WTe2 for low crystal symmetry to satisfy the above requirements. The PtTe2/WTe2 bilayers exhibit a high in-plane spin Hall conductivity σs,y ≈ 2.32 × 105 × h/2e Ω-1 m-1 and out-of-plane spin Hall conductivity σs,z ≈ 0.25 × 105 × h/2e Ω-1 m-1, where h is the reduced Planck's constant and e is the value of the elementary charge. The out-of-plane spins in PtTe2/WTe2 bilayers enable the deterministic switching of perpendicular magnetization at room temperature without magnetic fields, and the power consumption is 67 times smaller than that of the Pt control case. The high out-of-plane spin Hall conductivity is attributed to the conversion from in-plane spin to out-of-plane spin, induced by the crystal asymmetry of WTe2. Our work establishes a low-power perpendicular magnetization manipulation based on wafer-scale two-dimensional van der Waals heterostructures.

OPTN gene therapy increases autophagy and protects mitochondria in SOD1-G93A-expressing transgenic mice and cells.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by progressive motor neuron (MN) death. Mutation of the superoxide dismutase 1 (SOD1) gene, which results in abnormal protein aggregation, is one of the causes of familial ALS. Autophagic dysfunction occurs in SOD1-G93A mutant mice as the disease progresses, but the etiology of this disease is still unclear. Optineurin (OPTN) is an adaptor that is involved in autophagy and participates in aggrephagy and mitophagy. Previous studies have established that OPTN mutations contribute to diseases such as glaucoma and ALS. However, the function of OPTN in autophagy and mitophagy has not been intensively investigated in models of ALS. In this study, we assessed the beneficial effect of OPTN on autophagy and mitochondrial function by intrathecally injecting adeno-associated virus 9 (AAV9)-OPTN into SOD1-G93A transgenic mice and by administering lentivirus (LV)-OPTN to cells expressing the SOD1-G93A mutant protein. The expression of voltage-dependent anion channel 1 (VDAC1) was increased and autophagy was elevated after OPTN gene therapy, as shown by a lower level of p62 and a higher level of microtubule-associated protein 1A/1B-light chain 3 (LC3)-II. Moreover, using electron microscopy, we observed a hyperpolarized mitochondrial transmembrane potential and reversal of mitochondrial morphological abnormalities. Furthermore, the protein level of TANK-binding kinase 1 (TBK1) was increased, suggesting that mitophagy was increased. Our findings from both animal and cell line studies strongly suggest that OPTN gene therapy is a powerful strategy to increase autophagy and protect mitochondria to prevent the progression of ALS and could be effective in the treatment of ALS.

A case report of laparoscopic surgery for Mayer-Rokitansky-Küster-Hauser syndrome with preservation of functional primordial uterus.

BACKGROUND: In the past, the primary treatment for MRKH syndrome (Mayer-Rokitansky-Küster-Hauser syndrome) with a functional primordial uterus was surgical removal of the functional primordial uterus. In rare instances, the endometrium of the functional primordial uterus is well developed, and surgical preservation of the functional primordial uterus provides the possibility of preserving reproductive function for these patients. CASE PRESENTATION: A 14-year-old female was diagnosed with type I MRKH syndrome with a functional primordial uterus through physical examination and imaging investigations. We freed the functional primordial uterus through laparoscopic surgery and excised a portion of the lower myometrium to create an outlet at a lower uterine segment, which we then intermittently anastomosed to the tip of the artificial vagina. The patient recovered well after the surgery, and a re-examination showed no significant abnormalities. CONCLUSION: We were successful in preserving the functional primordial uterus using laparoscopic surgery in a patient with MRKH syndrome and connecting it to an artificial vagina through reconstructive surgery to ensure unobstructed menstrual drainage and preserve the reproductive potential of the patient.

Stratifin (SFN) Regulates Cervical Cancer Cell Proliferation, Apoptosis, and Cytoskeletal Remodeling and Metastasis Progression Through LIMK2/Cofilin Signaling.

The aberrant expression of Stratifin (SFN) is intricately associated with the initiation and progression of numerous tumors. This study aims to investigate whether SFN regulates the metastasis of cervical cancer cells through the LIMK2/Cofilin signaling pathway. In this study, we compared the expression of SFN in normal cervical tissues and cervical carcinoma tissues. We established SFN overexpression and SFN silencing cellular models to assess the invasive and migratory capabilities of cervical cancer cells using transwell and scratch assays. YO-PRO-1/PI and EdU staining were employed to evaluate apoptotic and proliferative capacities, while Actin-Tracker Green-488 was utilized to investigate cytoskeletal remodeling. The expression levels of SFN, LIMK2, p-LIMK2, Cofilin, and p-Cofilin were examined through Western blotting and immunofluorescence. Our findings revealed elevated expression of SFN in cervical squamous cell carcinoma tissues. SFN overexpression was observed to enhance invasion and migration of cervical cancer cells, induce cytoskeletal remodeling, facilitate cell proliferation, and suppress apoptosis. Furthermore, SFN overexpression upregulated the expression levels of LIMK2, p-LIMK2, Cofilin, and p-Cofilin. Conversely, silencing SFN exerted opposite effects. SFN plays an important role in the diagnosis of cervical cancer. SFN can regulate cervical cancer cell proliferation, apoptosis, cytoskeletal remodeling and metastasis through LIMK2/Cofilin signaling.

Preterm Birth and Infantile Appendicitis.

OBJECTIVE: To investigate the potential association between preterm birth and infantile appendicitis. METHODS: We conducted a retrospective, multicenter, matched case-control study. This study included consecutive patients <1 year of age with surgery- or autopsy-confirmed appendicitis, admitted between December 2007 and May 2023. For each case, 10 healthy infants were randomly selected and matched by age. Infants were categorized as neonates (0 to 28 days) or older infants (>28 days and <1 year). RESULTS: The study included 106 infants diagnosed with appendicitis (median age 2.4 months) and 1060 age-matched healthy controls. In the univariate analysis, preterm birth was significantly associated with the development of appendicitis within the first year of life (odds ratio [OR], 4.23; 95% confidence interval [CI], 2.67-6.70). Other factors associated with a higher risk of infantile appendicitis included being male (OR, 1.91; 95%CI, 1.25-2.94), weight-for-age z-score (OR, 0.72; 95%CI, 0.64-0.81), and exclusively fed on formula (OR, 2.95; 95%CI, 1.77-4.91). In multivariable analyses, preterm remained significantly associated with appendicitis (adjusted OR, 3.32; 95%CI, 1.76-6.24). Subgroup analysis revealed that a preterm birth history increased the risk of appendicitis in both neonates (adjusted OR, 4.56; 95%CI, 2.14-9.71) and older infants (adjusted OR, 3.63; 95%CI, 1.72-7.65). However, preterm did not significantly influence the incidence of appendiceal perforation. CONCLUSIONS: Preterm infants have an increased risk of appendicitis during the first year of life. A preterm birth history may help improve the timely diagnosis of infantile appendicitis.

The effect of family boundary flexibility on employees' work engagement: a study based on person-environment fit theory perspective.

Under the impact of the era of big data and public emergency, the blurring of family-work boundaries and the increasing burden of family responsibilities will pose a great challenge to employee resilience and family work balance, which in turn will affect employees' work engagement. Therefore, based on the person-environment fit theory, this study aims to explore the potential mechanism and boundary conditions of employee family boundary flexibility fit on work engagement. This study conducted a random sampling of enterprise employees in China. A sample of 433 participants completed a questionnaire to provide data. We conduct hierarchical regression and Bootstrap analysis to verify the hypothesis model. The study found that employees' work engagement is significantly improved when their family boundary flexibility is matched. Family-work enrichment plays a role in mediating the impact of employees' family boundary flexibility on work engagement. The relationship between family-work enrichment and work engagement is moderated by family support. Therefore, enterprises should respect and value each employee's family boundary flexibility, establish family-friendly policies, and consider personal family boundary flexibility in employees' career development planning. This will promote the enhancement of employee resilience, enable better engagement in work, improve work efficiency, and enhance the core competitiveness of enterprises.

Clinical features and treatment outcomes of infantile appendicitis: a multicentre study.

Appendicitis in infants is a life-threatening condition that is seldom studied. Our purpose was to conduct a comprehensive evaluation of appendicitis in this age group. This was a multicenter retrospective study. Patients aged under one year with surgically confirmed appendicitis during January, 2010 to May, 2022 were identified from four institutional databases. The patients were grouped as neonates or older infants based on their age at the onset of symptoms associated with acute appendicitis. The study encompassed 98 infants, with median age of 66.5 (IQR, 13.8-176.0) days. Neonates were more likely to exhibit abdominal distension (64.9%) and fever (56.8%), while older infants more frequently presented with fever (88.5%) and vomiting (49.2%). Most patients (76.5%) were misdiagnosed during their initial clinical encounter, with a -rate was 3.1% (3 deaths), with neonates exhibiting a rate of 5.4%, and older infants 1.6%. Compared to older infants, neonates showed a higher incidence of appendiceal perforation (OR, 2.9; 95%CI, 1.1-8.1), mechanical ventilation (OR, 9.5; 95%CI, 3.1-29.2), and ICU admission (OR, 16.1; 95%CI, 5.6-45.7). However, there were no significant differences in mortality rates, 30-day readmission rates, and surgical complications between the two groups. CONCLUSION: Although most infants with appendicitis were misdiagnosed during the first clinical encounter, the observed mortality rates were considerably lower than previously reported. While neonates and infants over 28 days displayed differing clinical presentations and disease severity, their outcomes were similar. WHAT IS KNOWN: • Appendicitis in infants is a critical yet underemphasized health concern, often misdiagnosed at initial clinical encounters due to its atypical presentation and non-specific symptoms. • The mortality rates in the neonates with appendicitis was 23% during the past decades. WHAT IS NEW: • The neonates and older infants displayed differing clinical presentations and disease severity. The treatment outcomes were similar. • The mortality rate for infantile appendicitis (3.1%) was significantly lower than historically reported.

The H protein of attenuated canine distemper virus is degraded via endoplasmic reticulum-associated protein degradation.

Canine distemper (CD) caused by canine distemper virus (CDV) is considered a highly contagious and acutely febrile disease in various animals around the world. Endoplasmic reticulum-associated protein degradation (ERAD) is an important biological effect induced by endoplasmic reticulum (ER) stress (ERS) for the degradation of unfolded/misfolded proteins in the ER of cells. CDV H glycoprotein is translocated into the ER for post-translational modifications. The effects of CDV H and ER on each other are unclear. In this study, we found that CDV H protein induced ERS through the PERK-mediated signaling pathway. The inhibition of ERS by 4-Phenylbutyric acid (4-PBA) increased the H protein amounts of an attenuated CDV, which was reduced by dithiothreitol (DTT)-induced ERS. Further, the H protein levels were increased when ERAD was inhibited by using Eeyarestatin I or interfering E3 ligase Hrd1 in ERAD, suggesting that the attenuated CDV H protein is degraded via ERAD. ERAD involved ubiquitin-dependent proteasome degradation (UPD) and/or autophagic-lysosome degradation (ALD). The attenuated CDV H protein was ubiquitinated and significantly increased after treatment with UPD inhibitor MG132 but not ALD inhibitor chloroquine (CQ), suggesting that ERAD degrading the attenuated CDV H protein selectively depends on UPD. Moreover, the inhibition of the degradation of CDV H protein with 4-PBA or MG132 treatment increased viral replication, whereas treatment with DTT promoting degradation of H protein was found to reduce viral replication. These findings suggest that the degradation of CDV H protein via ERAD negatively affects viral replication and provide a new idea for developing CDV prevention and control strategies.

Loss-of-Function of ATS1 Enhances Arabidopsis Salt Tolerance.

Despite the importance of lipid metabolism in various biological processes, little is known about the functionality of ATS1, a plastid glycerol-3-phosphate acyltransferase catalyzing the initial step of the prokaryotic glycerolipids biosynthetic pathway, in plant response to salt stress. In this study, both the loss-of-function mutants and the overexpression lines of ATS1 were analyzed for salt tolerance properties. The results showed that ATS1 overexpression lines had lower seed germination, shoot biomass, chlorophyll content, the proportion of relatively normal pod, and higher root/shoot ratio and anthocyanidin content compared with the wild type. Physiological and biochemical analysis revealed that ats1 mutants had more unsaturated fatty acids to stabilize the plasma membrane under salt damage. Additionally, less induction of three main antioxidant enzymes activity and lower MDA content in ats1 mutants indicated that mutation of the ATS1 gene could reduce the damage extent. Furthermore, the ats1 mutants maintained the K+/Na+ homeostasis by upregulating HAK5 expression to increase K+ absorption and down-regulating HKT1 expression to prevent Na+ uptake. This study suggested that the ATS1 gene negatively affects salt resistance in Arabidopsis.

High expression of NF-κB inducing kinase in the bulge region of hair follicle induces tumor.

The bulge region, a reservoir of multipotent stem cells, is possibly responsible for tumorigenesis. NF-κB-inducing kinase (NIK) is a kinase involved in the activation of the noncanonical NF-κB pathway and exhibits positive staining in tumor cells. However, whether high expression of NIK can result in tumorigenesis has not been reported in published papers. By establishing Nik-coe (Nik-stopF/F crossed with Chat-cre) and Nik-soe (Nik-stopF/F crossed with Sox9-cre) mice, we found that overexpression of Nik in the bulge region of hair follicles induced hair follicle loss and tumorigenesis. Furthermore, RNA sequencing, proteomic and phosphopeptide analyses revealed that multiple cancer pathways are involved in tumor formation. Taken together, these findings indicate that constitutive activation of Nik in the bulge region induces tumorigenesis.