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CLEC9A is a group V C-type lectin-like receptor (CTLR) that functions as an activation receptor and is expressed on myeloid lineage cells (Huysamen et al., 2008 [PubMed 18408006]).[supplied by OMIM, Aug 2008].. Additionally we are shipping CLEC9A Proteins (7) and CLEC9A Kits (2) and many more products for this protein.
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Human Monoclonal CLEC9A Primary Antibody for FACS - ABIN4897678
Balan, Ollion, Colletti, Chelbi, Montanana-Sanchis, Liu, Vu Manh, Sanchez, Savoret, Perrot, Doffin, Fossum, Bechlian, Chabannon, Bogen, Asselin-Paturel, Shaw, Soos, Caux, Valladeau-Guilemond, Dalod: Human XCR1+ dendritic cells derived in vitro from CD34+ progenitors closely resemble blood dendritic cells, including their adjuvant responsiveness, contrary to monocyte-derived dendritic cells. in Journal of immunology (Baltimore, Md. : 1950) 2014
Show all 2 Pubmed References
Clec9a is responsible for the antigen cross-presentation of dendritic cell subsets and may be a target of immunotherapy
findings demonstrate that CLEC9A is a specialized receptor that modulates the innate immune response when there is a mycobacterial infection
Data indicate that blood dendritic cell antigen 3 BDCA3 (show THBD Antibodies)(+) and C-type lectin (show MBL2 Antibodies) domain family 9, member A (show CXCL14 Antibodies) CLEC9A(+) dendritic cells (DC) are of major importance in the induction of anti-viral and anti-tumor immunity.
Activated dendritic cell subsets expressing CD141 (show THBD Antibodies)/CLEA9A/CD1c (show CD1C Antibodies), likely recruited into the tubulointerstitium, are positioned to play a role in the development of fibrosis and, thus, progression to chronic kidney disease.
study showsn that the DNGR-1 ligand is preserved from yeast to man and corresponds to the F-actin component of the cellular cytoskeleton; identification of F-actin as a DNGR-1 ligand suggests that cytoskeletal exposure is a universal sign of cell damage that can be targeted by the innate immune system to initiate immunity
High expression of DNGR-1 specifically and universally identifies a unique dendritic cells subset in mouse and humans.
propose that Clec9A provides targeted recruitment of the adaptive immune system during infection and can also be utilized to enhance immune responses generated by vaccines.
Data show that CLEC9A is only expressed on immature BDCA3 (show THBD Antibodies)(+) myeloid dendritic cells (mDCs).
For production of cytotoxic T cells, transge (show LY75 Antibodies)nic DEC-205 and Clec9A, but (show CLEC12A Antibodies)not Clec12A, are effective targets for antibody-mediated delivery of antigens for vaccination, although only in the presence of adjuvants.
A population of human dendritic cells (DC) that expresses DNGR-1 (CLEC9A) and high levels of BDCA3 (show THBD Antibodies) and resembles mouse CD8alpha+ DCs in phenotype and function, is characterized.
Clec9A and Clec12A exhibit different intrinsic capacities to elicit MHC I and MHC II presentation following direct antigen targeting
DNGR-1 also regulated Trm cell generation.
A specific deletion of DNGR-1 limits the development of atherosclerosis and vascular inflammation.
The authors describe a conformational change that occurs in the neck region of DNGR-1 in a pH- and ionic strength-dependent manner and that controls cross-presentation of dead cell-associated antigens.
Study found presence of DNGR-1 in the brain, providing a potential marker for the study of a specific denditritic brain cell subset
A dependence on DNGR-1 for RSV-specific CD8 (show CD8A Antibodies)(+) T-cell responses was observed.
Genetic tracing of DNGR-1 expression history specifically marks cells traditionally ascribed to the dendritic cells lineage, and this restriction is maintained after inflammation.
Clec9A-positive dendritic cells control susceptibility of mice to experimental cerebral malaria.
Loss of DNGR-1 impaired the CD8 (show CD8A Antibodies) positive lymphocyte cytotoxic response to vaccinia virus, especially against those virus strains that are most dependent on cross-presentation.
CLEC9A is a group V C-type lectin-like receptor (CTLR) that functions as an activation receptor and is expressed on myeloid lineage cells (Huysamen et al., 2008
C-type lectin domain family 9 member A
, dendritic cell natural killer lectin group receptor 1