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2 edition of Characterization of lineage-specific expression and signaling function of mouse NKR-P1 (CD161). found in the catalog.

Characterization of lineage-specific expression and signaling function of mouse NKR-P1 (CD161).

Belma Ljutic

Characterization of lineage-specific expression and signaling function of mouse NKR-P1 (CD161).

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Published .
Written in English


About the Edition

Furthermore, although it is known that the NK1.1 marker is encoded by the Nkrp1c gene, its transcriptional regulation has not been elucidated. The results presented in this thesis define the molecular basis of Nkrp1c expression in NK lineage cells. In particular, the location of the Nkrp1c transcriptional initiation site, a novel 5" untranslated exon, and the minimal functional core promoter have been identified. Furthermore, we describe the detection and analysis of a DNaseI hypersensitive site (HS1), located 9 kb upstream of the transcriptional initiation site, which exhibits NK cell-specific enhancer-like activity. Taken together, our findings identify the minimal elements necessary for conferring NK cell lineage-specific expression of the Nkrp1c gene. These findings set the stage for the further characterization of the DNA-binding factors responsible for the expression of this and other NK-specific genes, shedding light on our understanding of how NK cell functions are regulated.For over fifteen years, surface expression of the NK1.1 marker has been used to identify all cells belonging to a specific subset of lymphocytes, defining them as natural killer (NK) cells. NK1.1 epitope is shared by two closely related, but functionally opposing NK cell receptors, the stimulatory NKR-P1C and inhibitory NKR-P1B gene products. Thus, the molecular basis of NKR-P1B/C signaling in NK cells was investigated. In particular, the tyrosine kinase, Lck, was identified as the initiator of signaling for both the stimulatory and inhibitory NKR-P1 receptors. Furthermore, the amino acid motif (CxCP) was shown to mediate Lck association to the receptors, as well as the inhibitory motif (LxYxxL) responsible for their divergent functions. Most strikingly, the Lck tyrosine kinase is required for NKR-P1 activation, as NK cells from Lck-deficient mice cannot mediate NKR-P1-directed killing. Importantly, this discovery represents the first NK cell defect reported in these mice. These findings provide the foundation for a sequential model to explain the opposing functional outcomes induced by these two NKR-P1 receptors, shedding light on our understanding of how NK cell functions are regulated.

The Physical Object
Pagination183 leaves.
Number of Pages183
ID Numbers
Open LibraryOL19887128M
ISBN 100612943801


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Characterization of lineage-specific expression and signaling function of mouse NKR-P1 (CD161). by Belma Ljutic Download PDF EPUB FB2

Ljutic B, Carlyle JR, Zúñiga-Pflücker JC () Identification of upstream cis-acting regulatory elements controlling lineage-specific expression of the mouse NK cell activation receptor, NKR-P1C.

J Biol Chem – PubMed CrossRef Google ScholarAuthor: Rajesh K. Gupta, G. Gupta. W E Seaman's research works with 7, citations and 3, reads, including: New blood: Creative funding of disease-specifc research.

In common with NKR-P1 and LLT1, B-NK and B-lec are located next to each other and transcribed in opposite orientation. Like human NKR-P1, B-NK has a functional inhibitory signaling motif in the. Avian immunology is a fascinating and growing field and will surely provide new and exciting insights for mainstream immunology in the future.

REFERENCES Adelmann, H.B. The Embryological Treatises of Hieronymus Fabricius of Aquapendente. This banner text can have markup. web; books; video; audio; software; images; Toggle navigation. C-type lectin superfamily 2, member D (CLEC2D) / osteoclast inhibitory lectin (Ocil) / Clr-b / CLAX / LLT-1, a member of a previously cloned group of C-type lectin-related (Clr) proteins linked to the NKR-P1 receptors in the mouse NK gene complex (NKC).

Expression of Ocil/Clr-b on mouse tumor cell lines inhibits NK cell-mediated killing. We use cookies to enhance your experience on our website. By continuing to use our website, you are agreeing to our use of cookies.

You can change your cookie settings at any time. A catalogue record for this book is available from the British Library. This book on avian immunology is timely; it should play a key role by gathering together Avian Immunology. What is claimed is: 1. A method of screening a candidate agent for an activity that is potentially useful in treatment or prophylaxis of diseases involving angiogenic processes, wherein the activity is an enhancement, inhibition, or prevention of a formation or outgrowth of a blood vessel or a lymph vessel, and wherein the method comprises the steps of: (i) administering the agent to a teleost.

The expression vector is any of the mammalian, yeast, insect or bacterial expression systems known in the art. Commercially available vectors and expression systems are available from a variety of suppliers including Genetics Institute (Cambridge, Mass.), Stratagene (La Jolla, Calif.), Promega (Madison, Wis.), and Invitrogen (San Diego, Calif.).

Abstract. The primate immune system is the outcome of hundreds of millions of years of complex evolution. Its divergence from the immune systems of other species and variation within the order affect primate disease susceptibility, infectious disease emergence, and human by: 1.

The autonomous signaling is a function of CD4– CD8– thymocytes where the pre-TCR signaling takes place. At this time, the structural basis for the oligomerization of pre-TCRs is not known. Antigen Recognition Antigens are recognized by the immune system by utilizing antibodies generated by B cells and by TCR on the T cells.

Although the ligand for NKR-P1 (Karlhofer and Yokoyama, ) is unknown, the receptor is expressed on all NK cells from a number of mouse strains. Except for CD, these receptors function by association with adapter molecules, which contain ITAM motifs.

Transgenic expression of E2A (Singh & Pongubala, ), but not of EBF or PAX-5, or expression of important lineagespecific genes controlled by these early regulators (e.g., the IL7-receptor) (Choi et al., ) induce autonomous, environment-independent, B-lineage specific differentiation.4/5(1).