Nkrp1 Family, from Lectins to Protein Interacting Molecules

Rozbeský, Daniel; Ivanová, Ljubina; Hernychová, Lucie; Grobárová, Valéria; Novák, Petr; Černý, Jan

doi:10.3390/molecules20023463

Cited by 6 publications

(3 citation statements)

References 103 publications

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“…A variety of receptors expressed on NK cells can be divided into active receptors and inhibitory receptors. The active receptors belong to the characteristic natural cytotoxicity receptor (NCR) family, such as NKp46, NKp30, NKp44 [20,21], and C type lectin family receptor (NKG2D, CD94/NKG2C, CD94/NKG2E, CD94/NKG2F, and CD161) [22], and also include active KIRs (killer immunoglobulin receptors), such as KIR2DS1, KIR2DS4, and KIR2DL4 [23]. The inhibitory receptors mainly include NKG2A, KIR2DL1, KIR2DL2/L3, and KIR3DL1 [24,25].…”

Section: The Discovery Of Nkg2dmentioning

confidence: 99%

Recent Advances in Molecular Mechanisms of the NKG2D Pathway in Hepatocellular Carcinoma

Wang¹,

Li²,

Sun³

2020

Biomolecules

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Hepatocellular carcinoma is a common malignant tumor with high mortality. Its malignant proliferation, invasion, and metastasis are closely related to the cellular immune function of the patients. NKG2D is a key activated and type II membrane protein molecule expressed on the surface of almost all NK cells. The human NKG2D gene is 270 kb long, located at 12p12.3–p13.1, and contains 10 exons and 9 introns. The three-dimensional structure of the NKG2D monomeric protein contains two alpha-helices, two beta-lamellae, and four disulfide bonds, and its’ signal of activation is transmitted mainly by the adaptor protein (DAP). NKG2D ligands, including MICA, MICB, and ULBPs, can be widely expressed in hepatoma cells. After a combination of NKG2D and DAP10 in the form of homologous two polymers, the YxxM motif in the cytoplasm is phosphorylated and then signaling pathways are also gradually activated, such as PI3K, PLCγ2, JNK-cJunN, and others. Activated NK cells can enhance the sensitivity to hepatoma cells and specifically dissolve by releasing a variety of cytokines (TNF-α and IFN-γ), perforin, and high expression of FasL, CD16, and TRAIL. NK cells may specifically bind to the over-expressed MICA, MICB, and ULBPs of hepatocellular carcinoma cells through the surface activating receptor NKG2D, which can help to accurately identify hepatoma, play a critical role in anti-hepatoma via the pathway of cytotoxic effects, and obviously delay the poor progress of hepatocellular carcinoma.

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Section: The Discovery Of Nkg2dmentioning

confidence: 99%

Recent Advances in Molecular Mechanisms of the NKG2D Pathway in Hepatocellular Carcinoma

Wang¹,

Li²,

Sun³

2020

Biomolecules

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“…The LYSMD3 domain is a pattern recognition receptor that is capable of binding chitin and sensing it. Other pattern recognition receptors that have affinity to chitin and derivatives of chitin are FIBCD1, NKR-P1, RegIIIγ and galectin-3 [ 69 , 70 , 71 , 72 , 73 ].…”

Section: The Role Of Chitin and Its Derivativesmentioning

confidence: 99%

Dual Role of Chitin as the Double Edged Sword in Controlling the NLRP3 Inflammasome Driven Gastrointestinal and Gynaecological Tumours

et al. 2022

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The role of NLRP3 in the tumour microenvironment is elusive. In some cancers, the activation of NLRP3 causes a worse prognosis and in some cancers, NLRP3 increases chances of survivability. However, in many cases where NLRP3 has a protumorigenic role, inhibition of NLRP3 would be a crucial step in therapy. Consequently, activation of NLRP3 would be of essence when inflammation is required. Although many ways of inhibiting and activating NLRP3 in cancers have been discussed before, not a lot of focus has been given to chitin and chitosan in this context. The availability of these marine compounds and their versatility in dealing with inflammation needs to be investigated further in relation with cancers, along with other natural extracts. In this review, the effects of NLRP3 on gastrointestinal and gynaecological cancers and the impact of different natural extracts on NLRP3s with special emphasis on chitin and chitosan is discussed. A research gap in using chitin derivatives as anti/pro-inflammatory agents in cancer treatment has been highlighted.

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“…Natural killer cell surface protein P1A (NKRP1A/CD161) is a family of receptors with both activating and inhibitory properties, expressed mostly on natural killer (NK) cells as well as on T lymphocytes and dendritic cells (DC) [ 9 , 10 ]. In mice, the following receptors within the NKRP1A family can be distinguished: NK-RP1A, NKp80, and NKp65, while in humans the only receptor is NKRP1A [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

PECAM-1 Is Down-Regulated in γδT Cells during Remission, but Up-Regulated in Relapse of Multiple Sclerosis

Zarobkiewicz

Morawska

Kowalska

et al. 2022

JCM

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Introduction. PECAM-1 and NKRP1A are both involved in the vascular transmigration of T lymphocytes. Vascular transmigration is a crucial process in multiple sclerosis pathogenesis. Methods and aim. The current paper presents an analysis of PECAM-1 and NKRP1A expression on γδ T cells. Expression of PECAM-1 and NKRP1A on subsets of γδ T cells was performed with flow cytometry. Results. Based on the flow cytometry data, PECAM1 was slightly differentially modulated on γδ T cells—it was up-regulated during relapse, but down-regulated during remission. Moreover, a significant downregulation of CD3 expression was noted on γδ T cells from MS patients, most notably during relapse. Conclusions. This may be a sign of the overall activation of γδ T cells in the course of multiple sclerosis.

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Nkrp1 Family, from Lectins to Protein Interacting Molecules

Cited by 6 publications

References 103 publications

Recent Advances in Molecular Mechanisms of the NKG2D Pathway in Hepatocellular Carcinoma

Recent Advances in Molecular Mechanisms of the NKG2D Pathway in Hepatocellular Carcinoma

Dual Role of Chitin as the Double Edged Sword in Controlling the NLRP3 Inflammasome Driven Gastrointestinal and Gynaecological Tumours

PECAM-1 Is Down-Regulated in γδT Cells during Remission, but Up-Regulated in Relapse of Multiple Sclerosis

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