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10.1016/j.jaci.2015.06.031 http://scihub22266oqcxt.onion/10.1016/j.jaci.2015.06.031 C4894862!4894862 !26277595     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26277595 &cmd=llinks): Failed to open stream: HTTP request failed! 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Genetic errors of the human caspase recruitment domain-B-cell lymphoma 10-mucosa-associated lymphoid tissue lymphoma-translocation gene 1 (CBM) complex: Molecular, immunologic, and clinical heterogeneity |pdf=|usr=}}{{26277595 }} gab.com Text Genetic errors of the human caspase recruitment domain-B-cell lymphoma 10-mucosa-associated lymphoid tissue lymphoma-translocation gene 1 (CBM) complex: Molecular, immunologic, and clinical heterogeneity JO: J Allergy Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26277595 #FOAvip Three members of the caspase recruitment domain (CARD) family of adaptors (CARD9, CARD10, and CARD11) are known to form heterotrimers with B-cell lymphoma 10 (BCL10) and mucosa-associated lymphoid tissue lymphoma-translocation gene 1 (MALT1). These 3 CARD-BCL10-MALT1 (CBM) complexes activate nuclear factor ?B in both the innate and adaptive arms of immunity. Human inherited defects of the 3 components of the CBM complex, including the 2 adaptors CARD9 and CARD11 and the 2 core components BCL10 and MALT1, have recently been reported. Biallelic loss-of-function mutant alleles underlie several different immunologic and clinical phenotypes, which can be assigned to 2 distinct categories. Isolated invasive fungal infections of unclear cellular basis are associated with CARD9 deficiency, whereas a broad range of clinical manifestations, including those characteristic of T- and B-lymphocyte defects, are associated with CARD11, MALT1, and BCL10 deficiencies. Interestingly, human subjects with these mutations have some features in common with the corresponding knockout mice, but other features are different between human subjects and mice. Moreover, germline and somatic gain-of-function mutations of MALT1, BCL10, and CARD11 have also been found in patients with other lymphoproliferative disorders. This broad range of germline and somatic CBM lesions, including loss-of-function and gain-of-function mutations, highlights the contribution of each of the components of the CBM complex to human immunity. Twit Text FOAVip Genetic errors of the human caspase recruitment domain-B-cell lymphoma 10-mucosa-associated lymphoid tissue lymphoma-translocation gene 1 (CBM) complex: Molecular, immunologic, and clinical heterogeneity ????J Allergy Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26277595 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26277595 #FOAvip English Wikipedia <ref>{{Cite pmid|26277595 }}</ref> Genetic errors of the human caspase recruitment domain-B-cell lymphoma 10-mucosa-associated lymphoid tissue lymphoma-translocation gene 1 (CBM) complex: Molecular, immunologic, and clinical heterogeneity #MMPMID26277595 Pérez de Diego R ; Sánchez-Ramón S ; López-Collazo E ; Martínez-Barricarte R ; Cubillos-Zapata C ; Ferreira Cerdán A ; Casanova JL ; Puel A J Allergy Clin Immunol 2015[Nov]; 136 (5 ): 1139-49 PMID26277595 show ga Three members of the caspase recruitment domain (CARD) family of adaptors (CARD9, CARD10, and CARD11) are known to form heterotrimers with B-cell lymphoma 10 (BCL10) and mucosa-associated lymphoid tissue lymphoma-translocation gene 1 (MALT1). These 3 CARD-BCL10-MALT1 (CBM) complexes activate nuclear factor ?B in both the innate and adaptive arms of immunity. Human inherited defects of the 3 components of the CBM complex, including the 2 adaptors CARD9 and CARD11 and the 2 core components BCL10 and MALT1, have recently been reported. Biallelic loss-of-function mutant alleles underlie several different immunologic and clinical phenotypes, which can be assigned to 2 distinct categories. Isolated invasive fungal infections of unclear cellular basis are associated with CARD9 deficiency, whereas a broad range of clinical manifestations, including those characteristic of T- and B-lymphocyte defects, are associated with CARD11, MALT1, and BCL10 deficiencies. Interestingly, human subjects with these mutations have some features in common with the corresponding knockout mice, but other features are different between human subjects and mice. Moreover, germline and somatic gain-of-function mutations of MALT1, BCL10, and CARD11 have also been found in patients with other lymphoproliferative disorders. This broad range of germline and somatic CBM lesions, including loss-of-function and gain-of-function mutations, highlights the contribution of each of the components of the CBM complex to human immunity. |Adaptive Immunity [MESH] |Adaptor Proteins, Signal Transducing/*genetics/metabolism [MESH] |Animals [MESH] |B-Cell CLL-Lymphoma 10 Protein [MESH] |CARD Signaling Adaptor Proteins/*genetics/metabolism [MESH] |Caspases/*genetics/metabolism [MESH] |Genetic Predisposition to Disease [MESH] |Guanylate Cyclase/genetics [MESH] |Humans [MESH] |Immunity, Innate [MESH] |Immunologic Deficiency Syndromes/*genetics [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein [MESH] |Mutation/genetics [MESH] |Mycoses/*genetics [MESH] |Neoplasm Proteins/*genetics/metabolism [MESH]Genetic errors of the human caspase recruitment domain-B-cell lymphoma(epmc).pdf DeepDyve Pubget Overpricing