The Bcr N-terminal oligomerization domain contributes to the full oncogenicity of P190 Bcr/Abl in transgenic mice.

International journal of molecular medicine

Volumn 7, Issue 4, 2001, Pages 351-357

  Heisterkamp, N ^a   Voncken, J W ^a   Senadheera, D ^a   Hemmeryckx, B ^a   Gonzalez Gomez, I ^a   Reichert, A ^a   Pattengale, P K ^a   Groffen, J ^a  

^a CHILDREN S HOSPITAL LOS ANGELES   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BCR ABL PROTEIN; BCR PROTEIN, MOUSE; BREAKPOINT CLUSTER REGION PROTEIN; ONCOPROTEIN; PEPTIDE FRAGMENT; PROTEIN TYROSINE KINASE;

ACUTE LYMPHOCYTIC LEUKEMIA; ANIMAL; ARTICLE; EXPERIMENTAL LEUKEMIA; GENE DELETION; GENE EXPRESSION REGULATION; GENETICS; MOUSE; PHYSIOLOGY; PROTEIN TERTIARY STRUCTURE; TRANSGENIC MOUSE;

ANIMALS; FUSION PROTEINS, BCR-ABL; GENE EXPRESSION REGULATION, LEUKEMIC; LEUKEMIA, EXPERIMENTAL; LEUKEMIA, LYMPHOCYTIC, ACUTE; MICE; MICE, TRANSGENIC; ONCOGENE PROTEINS; PEPTIDE FRAGMENTS; PROTEIN STRUCTURE, TERTIARY; PROTEIN-TYROSINE KINASES; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-BCR; SEQUENCE DELETION;

MLCS; MLOWN;

EID: 0035318307     PISSN: 11073756     EISSN: None     Source Type: Journal    
DOI: 10.3892/ijmm.7.4.351     Document Type: Article

References (0)