A Bioinformatics Resource for TWEAK-Fn14 Signaling Pathway

Bhattacharjee, Mitali; Raju, Rajesh; Radhakrishnan, Aneesha; Nanjappa, Vishalakshi; Muthusamy, Babylakshmi; Singh, Kulwant; Kuppusamy, Dheebika; Lingala, Bhavya Teja; Pan, Archana; Mathur, P. B.; Harsha, H. C.; Prasad, T. S. Keshava; Atkins, Gerald J.; Pandey, Akhilesh; Chatterjee, Aditi

doi:10.1155/2012/376470

Cited by 26 publications

(31 citation statements)

References 78 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…TNFRSF12A was up-regulated by loading both days. It is a cell surface receptor and thought to be a major physiologic mediator of tissue repair after acute injury by regulating inflammation, tissue remodeling, migration, differentiation, apoptosis and angiogenesis (4,9). Interestingly, TNFRSF12A specifically promotes proliferation and increases collagen production in fibroblasts (9).…”

Section: Genes Regulated Both Days Might Affect Inflammation Extracementioning

confidence: 99%

Different gene response to mechanical loading during early and late phases of rat Achilles tendon healing

Hammerman

Blomgran

Dansac

et al. 2017

Journal of Applied Physiology

View full text Add to dashboard Cite

Mechanical loading stimulates tendon healing both when applied in the inflammatory phase and in the early remodeling phase of the process, although not necessarily via the same mechanisms. We investigated the gene response to mechanical loading in these two phases of tendon healing. The right Achilles tendon in rats was transected, and the hindlimbs were unloaded by tail suspension. The rats were exposed to 5 min of treadmill running 3 or 14 days after tendon transection. Thereafter, they were resuspended for 15 min or 3 h until euthanasia. The controls were suspended continuously. Gene analysis was first performed by microarray analysis followed by quantitative RT-PCR on selected genes, focusing on inflammation. Fifteen minutes after loading, the most important genes seemed to be the transcription factors EGR1 and C-FOS, regardless of healing phase. These transcription factors might promote tendon cell proliferation and differentiation, stimulate collagen production, and regulate inflammation. Three hours after loading on , inflammation was strongly affected. Seven inflammation-related genes were upregulated according to PCR: CCL20, CCL7, IL-6, NFIL3, PTX3, SOCS1, and TLR2. These genes can be connected to macrophages, T cells, and recruitment of leukocytes. According to Ingenuity Pathway Analysis, the recruitment of leukocytes was increased by loading on, which also was confirmed by histology. This inflammation-related gene response was not seen on Our results suggest that the immediate gene response after mechanical loading is similar in the early and late phases of healing but the late gene response is different. This study investigates the direct effect of mechanical loading on gene expression during different healing phases in tendon healing. One isolated episode of mechanical loading was studied in otherwise unloaded healing tendons. This enabled us to study a time sequence, i.e., which genes were the first ones to be regulated after the loading episode.

show abstract

Section: Genes Regulated Both Days Might Affect Inflammation Extracementioning

confidence: 99%

Different gene response to mechanical loading during early and late phases of rat Achilles tendon healing

Hammerman

Blomgran

Dansac

et al. 2017

Journal of Applied Physiology

View full text Add to dashboard Cite

show abstract

“…We screened published research articles related to TIE2 signaling. NetPath criteria described earlier [ 47 , 48 ] were followed for the annotation of protein-protein interactions (PPIs), enzyme-substrate relationships, and posttranslational modifications (PTMs) (catalytic events). Activation/inhibition status of proteins, alterations in protein localization, and also genes regulated at mRNA level by TIE2 signaling were also documented.…”

Section: Methodsmentioning

confidence: 99%

Signaling Network Map of Endothelial TEK Tyrosine Kinase

Khan

Sandhya

Singh

et al. 2014

Journal of Signal Transduction

Self Cite

View full text Add to dashboard Cite

TEK tyrosine kinase is primarily expressed on endothelial cells and is most commonly referred to as TIE2. TIE2 is a receptor tyrosine kinase modulated by its ligands, angiopoietins, to regulate the development and remodeling of vascular system. It is also one of the critical pathways associated with tumor angiogenesis and familial venous malformations. Apart from the vascular system, TIE2 signaling is also associated with postnatal hematopoiesis. Despite the involvement of TIE2-angiopoietin system in several diseases, the downstream molecular events of TIE2-angiopoietin signaling are not reported in any pathway repository. Therefore, carrying out a detailed review of published literature, we have documented molecular signaling events mediated by TIE2 in response to angiopoietins and developed a network map of TIE2 signaling. The pathway information is freely available to the scientific community through NetPath, a manually curated resource of signaling pathways. We hope that this pathway resource will provide an in-depth view of TIE2-angiopoietin signaling and will lead to identification of potential therapeutic targets for TIE2-angiopoietin associated disorders.

show abstract

“…Several studies have confirmed the therapeutic potential of this pathway in human esophageal and pancreatic cancers (21), autoimmune disorders (22), muscle atrophy and injury (23), and chemokinedependent inflammatory kidney disease (24). The ever increasing knowledge and data on various downstream reactions stimulated by TWEAK-Fn14 interaction has recently been compiled into a complete repository (25). This paves the way for identification of yet unknown components of the signaling pathways.…”

Section: Tweakmentioning

confidence: 98%

Structural Basis and Targeting of the Interaction between Fibroblast Growth Factor-inducible 14 and Tumor Necrosis Factor-like Weak Inducer of Apoptosis

Dhruv

Loftus

Narang

et al. 2013

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Aberrant TNF-like weak inducer of apoptosis (TWEAK)-fibroblast growth factor-inducible 14 (Fn14) signaling is observed in inflammation, autoimmune diseases, and cancers. Results: An integrated computational and experimental study identified small molecule inhibitors of TWEAK-Fn14 interaction. Conclusion:The TWEAK-Fn14 interaction is tractable and can be inhibited by small molecules. Significance: This is the first evidence of small molecules targeting TWEAK-Fn14 signaling.

show abstract

A Bioinformatics Resource for TWEAK-Fn14 Signaling Pathway

Cited by 26 publications

References 78 publications

Different gene response to mechanical loading during early and late phases of rat Achilles tendon healing

Different gene response to mechanical loading during early and late phases of rat Achilles tendon healing

Signaling Network Map of Endothelial TEK Tyrosine Kinase

Structural Basis and Targeting of the Interaction between Fibroblast Growth Factor-inducible 14 and Tumor Necrosis Factor-like Weak Inducer of Apoptosis

Contact Info

Product

Resources

About