about
BCR sequences essential for transformation by the BCR-ABL oncogene bind to the ABL SH2 regulatory domain in a non-phosphotyrosine-dependent mannerNon-hematopoietic expression of IDO is integrally required for inflammatory tumor promotionInhibition of indoleamine 2,3-dioxygenase, an immunoregulatory target of the cancer suppression gene Bin1, potentiates cancer chemotherapy.Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors.Indoleamine 2,3-dioxygenase is the anticancer target for a novel series of potent naphthoquinone-based inhibitors.Indoleamine 2,3-dioxygenase in T-cell tolerance and tumoral immune escape.Chronic inflammation that facilitates tumor progression creates local immune suppression by inducing indoleamine 2,3 dioxygenase.Indoleamine 2,3-dioxygenase in cancer: targeting pathological immune tolerance with small-molecule inhibitors.Oncogenic activation of c-ABL by mutation within its last exon.Indoleamine 2,3-dioxygenase in immune suppression and cancer.Structure-activity study of brassinin derivatives as indoleamine 2,3-dioxygenase inhibitors.The immunoregulatory enzyme IDO paradoxically drives B cell-mediated autoimmunity.Zinc protoporphyrin IX stimulates tumor immunity by disrupting the immunosuppressive enzyme indoleamine 2,3-dioxygenase.Targeted disruption of the murine Bin1/Amphiphysin II gene does not disable endocytosis but results in embryonic cardiomyopathy with aberrant myofibril formation.Tyrosine kinase activity and transformation potency of bcr-abl oncogene products.Beyond immunosuppression: reconsidering indoleamine 2,3-dioxygenase as a pathogenic element of chronic inflammation.A Sub-Type of Familial Pancreatic Cancer: Evidence and Implications of Loss of Function Polymorphisms and Indoleamine-2,3-Dioxygenase-2.Indoleamine 2,3-Dioxygenase and Its Therapeutic Inhibition in Cancer.The gas5 gene is disrupted by a frameshift mutation within its longest open reading frame in several inbred mouse strains and maps to murine chromosome 1.Bin3 deletion causes cataracts and increased susceptibility to lymphoma during aging.Inhibiting IDO pathways to treat cancer: lessons from the ECHO-301 trial and beyondIndoximod: An Immunometabolic Adjuvant That Empowers T Cell Activity in CancerBin1 ablation in mammary gland delays tissue remodeling and drives cancer progressionCardiac-specific disruption of Bin1 in mice enables a model of stress- and age-associated dilated cardiomyopathyHost IDO2 Gene Status Influences Tumor Progression and Radiotherapy Response in KRAS-Driven Sporadic Pancreatic Cancers
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description
researcher ORCID ID = 0000-0001-7854-6933
@en
wetenschapper
@nl
name
Alexander J Muller
@ast
Alexander J Muller
@en
Alexander J Muller
@es
Alexander J Muller
@nl
type
label
Alexander J Muller
@ast
Alexander J Muller
@en
Alexander J Muller
@es
Alexander J Muller
@nl
prefLabel
Alexander J Muller
@ast
Alexander J Muller
@en
Alexander J Muller
@es
Alexander J Muller
@nl
P1153
7404065102
P31
P496
0000-0001-7854-6933