Correction to: A De Novo Frameshift Mutation in TNFAIP3 Impairs A20 Deubiquitination Function to Cause Neuropsychiatric Systemic Lupus Erythematosus

Duan, Ruonan; Liu, Qi; Li, Jiangxia; Bian, Xianli; Yuan, Qianqian; Li, Yan; Feng, Lei; Gao, Shang; Wei, Shijun; Li, Pengyu; Gao, Fei; Sun, Wenjie; Li, Xi; Liu, Qiji

doi:10.1007/s10875-020-00838-y

Cited by 2 publications

(1 citation statement)

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“…It is both deubiquitinating and is an ubiquitin ligase. The vital involvement of this protein in regulating inflammatory signal transduction [15,16] to negatively regulate the NF-κB pathway via feedback and inhibit NF-κB pathway activation via several inflammatory signals has been shown [17][18][19][20]. It can inhibit the transcription of downstream inflammatory factors and has a strong anti-inflammatory effect.…”

Section: Discussionmentioning

confidence: 99%

Effects of Upregulation of TNFAIP3 on Diabetic Neuropathic Pain in Mice

Liu

Yao

et al. 2021

Disease Markers

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Globally, diabetes has assumed epidemic proportions with the neuropathic complications attributed to the malady emerging as a substantial burden on patients and society. DNP has greatly affected the daily life of patients, the effect of traditional treatment methods is not ideal, and it is easy to produce drug resistance. This work is aimed at scrutinizing the effect of upregulating the expression of TNFAIP3 on diabetic neuralgia in mice. This work entailed ascertaining the effects of TNFAIP3 on a murine DNP system. This inspired us to observe the analgesic effect via high expression of lentivirus-mediated TNFAIP3 by intrathecal injection in the animal model to explore its regulatory impacts, symptom relief, and mechanistic role in pain. The results displayed an attenuation of hind paw pain hypersensitivity by LV-TNFAIP3 in the animals. The spinal cord and dorsal root ganglion of mice with neuropathic pain displayed an evident dip in TNFAIP3. Inhibition of the ERK/NF-κB signaling pathway employing LV-TNFAIP3 conspicuously suppressed this pathway while the diabetic pain hypersensitivity was quelled. This effect was also seen with insulin treatment evidently. In conclusion, according to the above analyses, the interaction between DNP and extracellular signal-regulated kinase signal transduction pathway is one of the key factors of pathogenesis.

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