3qs9: Difference between revisions

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-[[Image:3qs9.png|left|200px]]
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 {{STRUCTURE_3qs9|  PDB=3qs9  |  SCENE=  }}
 ===Crystal structure of a human Flt3 ligand-receptor ternary complex===
+{{ABSTRACT_PUBMED_21389326}}
+==Disease==
+[[http://www.uniprot.org/uniprot/FLT3_HUMAN FLT3_HUMAN]] Defects in FLT3 are a cause of acute myelogenous leukemia (AML) [MIM:[http://omim.org/entry/601626 601626]]. AML is a malignant disease in which hematopoietic precursors are arrested in an early stage of development. Note=Somatic mutations that lead to constitutive activation of FLT3 are frequent in AML patients. These mutations fall into two classes, the most common being in-frame internal tandem duplications of variable length in the juxtamembrane region that disrupt the normal regulation of the kinase activity. Likewise, point mutations in the activation loop of the kinase domain can result in a constitutively activated kinase.<ref>PMID:11090077</ref><ref>PMID:16266983</ref><ref>PMID:14504097</ref><ref>PMID:9737679</ref><ref>PMID:18305215</ref><ref>PMID:11290608</ref><ref>PMID:8946930</ref><ref>PMID:11442493</ref>
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+==Function==
-The line below this paragraph, {{ABSTRACT_PUBMED_21389326}}, adds the Publication Abstract to the page
+[[http://www.uniprot.org/uniprot/FLT3L_HUMAN FLT3L_HUMAN]] Stimulates the proliferation of early hematopoietic cells by activating FLT3. Synergizes well with a number of other colony stimulating factors and interleukins. [[http://www.uniprot.org/uniprot/FLT3_HUMAN FLT3_HUMAN]] Tyrosine-protein kinase that acts as cell-surface receptor for the cytokine FLT3LG and regulates differentiation, proliferation and survival of hematopoietic progenitor cells and of dendritic cells. Promotes phosphorylation of SHC1 and AKT1, and activation of the downstream effector MTOR. Promotes activation of RAS signaling and phosphorylation of downstream kinases, including MAPK1/ERK2 and/or MAPK3/ERK1. Promotes phosphorylation of FES, FER, PTPN6/SHP, PTPN11/SHP-2, PLCG1, and STAT5A and/or STAT5B. Activation of wild-type FLT3 causes only marginal activation of STAT5A or STAT5B. Mutations that cause constitutive kinase activity promote cell proliferation and resistance to apoptosis via the activation of multiple signaling pathways.<ref>PMID:7507245</ref><ref>PMID:10080542</ref><ref>PMID:11090077</ref><ref>PMID:16266983</ref><ref>PMID:16627759</ref><ref>PMID:18490735</ref><ref>PMID:20111072</ref><ref>PMID:21067588</ref><ref>PMID:21262971</ref><ref>PMID:21516120</ref><ref>PMID:14504097</ref>
-(as it appears on PubMed at http://www.pubmed.gov), where 21389326 is the PubMed ID number.
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-{{ABSTRACT_PUBMED_21389326}}
 ==About this Structure==
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 ==Reference==
-<ref group="xtra">PMID:021389326</ref><ref group="xtra">PMID:019184382</ref><references group="xtra"/>
+<ref group="xtra">PMID:021389326</ref><ref group="xtra">PMID:019184382</ref><references group="xtra"/><references/>
 [[Category: Homo sapiens]]
 [[Category: Receptor protein-tyrosine kinase]]