FK506-binding protein-like and FK506-binding protein 8 regulate dual leucine zipper kinase degradation and neuronal responses to axon injury

Lee, Bohm; Oh, Yeonsoo; Cho, Eunhye; DiAntonio, Aaron; Cavalli, Valeria; Shin, Jung Eun; Choi, Hae Woong; Cho, Yongcheol

doi:10.1016/j.jbc.2022.101647

Cited by 10 publications

(9 citation statements)

References 38 publications

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“…It has been reported that the inhibition of DLK activation could delay axonal degeneration after both axotomy and chemotherapeutic treatment [33]. In agreement with this findings, a recent study showed that the in vivo overexpression of the DLK-interacting protein FK506-binding protein 8 (FKBP8) delayed the progression of axon degeneration and suppressed neuronal death through the regulation of DLK stability via the UPS and lysosomal protein degradation pathways [34]. Once the axon is damaged, NMNAT2 reduction or SARM1 activation induces calcium influx that starts the calcium-dependent calpain degradation of the axon, in which the active role of SARM1 is confirmed in human derived sensory neurons models of traumatic and neurotoxic degeneration [35].…”

Section: Axon Degenerationsupporting

confidence: 53%

Ubiquitin Proteasome System and Microtubules Are Master Regulators of Central and Peripheral Nervous System Axon Degeneration

Cartelli

Cavaletti

Lauria

et al. 2022

Cells

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Axonal degeneration is an active process that differs from neuronal death, and it is the hallmark of many disorders affecting the central and peripheral nervous system. Starting from the analyses of Wallerian degeneration, the simplest experimental model, here we describe how the long projecting neuronal populations affected in Parkinson’s disease and chemotherapy-induced peripheral neuropathies share commonalities in the mechanisms and molecular players driving the earliest phase of axon degeneration. Indeed, both dopaminergic and sensory neurons are particularly susceptible to alterations of microtubules and axonal transport as well as to dysfunctions of the ubiquitin proteasome system and protein quality control. Finally, we report an updated review on current knowledge of key molecules able to modulate these targets, blocking the on-going axonal degeneration and inducing neuronal regeneration. These molecules might represent good candidates for disease-modifying treatment, which might expand the window of intervention improving patients’ quality of life.

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Section: Axon Degenerationsupporting

confidence: 53%

Ubiquitin Proteasome System and Microtubules Are Master Regulators of Central and Peripheral Nervous System Axon Degeneration

Cartelli

Cavaletti

Lauria

et al. 2022

Cells

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“…International Publisher inhibition of angiogenesis [9,10]. Recently, FKBPL is described as a dual leucine zipper kinase (DLK)-interacting protein that regulates DLK degradation via the lysosome and neuronal responses to axon injury [7]. Lin et al [11] reported that miR-183-5p promotes the proliferation and migration of vascular smooth muscle cells by reducing FKBPL expression.…”

Section: Ivyspringmentioning

confidence: 99%

“…FK506-binding protein like (FKBPL) belongs to the immunophilin protein family, a group of conserved proteins binding to immunosuppressive drugs, such as FK506, rapamycin, and cyclosporin A 6 , 7 . Immunophilins are involved in many cellular processes, such as cell signalling, cell cycle progression, metabolic activity and apoptosis 8 .…”

Section: Introductionmentioning

confidence: 99%

“…FKBPL has been shown to play a critical role in regulating estrogen receptor (ER), androgen receptor (AR), glucocorticoid receptor (GR) and inflammatory signalling, cancer stem cell differentiation, and inhibition of angiogenesis 9 , 10 . Recently, FKBPL is described as a dual leucine zipper kinase (DLK)-interacting protein that regulates DLK degradation via the lysosome and neuronal responses to axon injury 7 . Lin et al 11 reported that miR-183-5p promotes the proliferation and migration of vascular smooth muscle cells by reducing FKBPL expression.…”

Section: Introductionmentioning

confidence: 99%

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Expression and role of FKBPL in lung adenocarcinoma

She,

Zhang,

Shen

et al. 2024

J. Cancer

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Dysregulated expression of FK506-binding protein like (FKBPL) has been demonstrated to play crucial roles in tumour development. However, the role of FKBPL in lung adenocarcinoma (ADC) remains unclear. Using immunohistochemical staining, we showed that FKBPL expression was significantly lower in lung ADC than the normal tissues ( P < 0.0001). Patients with well or moderately differentiated tumours have higher FKBPL expression compared with patients with poor differentiated tumours ( P = 0.037). However, no significant associations were found between FKBPL expression and other clinicopathological variables ( P > 0.05 for all). Cox univariate analysis showed that high FKBPL expression was correlated with prolonged overall survival (OS) ( P = 0.010). Kaplan-Meier analysis further confirmed that the FKBPL-low group showed a significantly shorter OS than the FKBPL-high group ( P = 0.0081). FKBPL expression was not shown as an independent prognostic factor for OS in the multivariate analysis ( P = 0.063). Moreover, our study demonstrated that FKBPL could suppress the proliferation of lung ADC cells by delaying cell cycle G1/S phase transition. In addition, FKBPL resulted in increased apoptosis in lung ADC cells. Using the Human Apoptosis Array Kit, we observed that overexpression of FKBPL in lung ADC A549 cells significantly decreased the anti-apoptotic proteins, including heat shock protein 32 (HSP32), heat shock protein 27 (HSP27), and paraoxonase-2 (PON2). FKBPL depletion significantly attenuated the pro-apoptotic protein, phospho-p53 (S46), in lung ADC H1975 cells. These new findings provide an experimental basis for further theoretical investigation of lung ADC.

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“…5 Tacrolimus exerts its action by binding to a protein named FK506 binding protein (FKBP) and inhibits the phosphatase function of calcineurin. 6,7 Calcineurin dephosphorylates the nuclear factor of activated T cells (NF-AT) which is a transcription factor and promotes the production of IL2 and other inflammatory cytokines. 8 Tacrolimus avoids the transcription of IL2 and the other cytokines of T lymphocytes by inhibition of calcineurin (Figure 1).…”

Section: Introductionmentioning

confidence: 99%

Stability Tests and Analytical Methods of Tacrolimus: A Review

Sajjadi,

Siahi-Shadbad,

Afshar Mogaddam

2022

ImmunoAnalysis

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Tacrolimus is an immunosuppressive drug widely used in organ or tissue transplantation. Furthermore, its anti-inflammatory effects are employed in treatments for psoriasis, uveitis, and vernal keratoconjunctivitis. According to the structural characteristics of tacrolimus, different transformations can be occurred on the drug and produces degradation products. Thus, stability and stress tests have a key role in the quality of tacrolimus with a narrow therapeutic index. Up to now, different studies have been developed for the study of tacrolimus stability under different conditions, and the degradation products were detected by different analytical instruments. Therefore, in the current study, available studies about tacrolimus degradation were collected and categorized into five main parts including acidic hydrolysis, alkaline hydrolysis, thermal, oxidative, and photolytic for better survey. The known degradation products with their chemical structures were also discussed in this study. Moreover, the analytical methods that are applied for drug characterization during stability tests were explained.

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FK506-binding protein-like and FK506-binding protein 8 regulate dual leucine zipper kinase degradation and neuronal responses to axon injury

Cited by 10 publications

References 38 publications

Ubiquitin Proteasome System and Microtubules Are Master Regulators of Central and Peripheral Nervous System Axon Degeneration

Ubiquitin Proteasome System and Microtubules Are Master Regulators of Central and Peripheral Nervous System Axon Degeneration

Expression and role of FKBPL in lung adenocarcinoma

Stability Tests and Analytical Methods of Tacrolimus: A Review

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