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Abetalipoproteinemia

Known as: Acanthocytosis, MTP DEFICIENCY, Microsomal Triglyceride Transfer Protein Deficiency Disease 
An autosomal recessive disorder of lipid metabolism. It is caused by mutation of the microsomal triglyceride transfer protein that catalyzes the… 
National Institutes of Health

Related topics

Related topics

21 relations
AcanthocytosisApolipoproteins BAtaxiaAutosomal recessive inheritance

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Wolman Disease with Hypolipoproteinemia and Acanthocytosis

Papers overview

Semantic Scholar uses AI to extract papers important to this topic.
Highly Cited
2011
Highly Cited
2011
Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity.
Imatinib therapy, which targets the oncogene product BCR-ABL, has transformed chronic myeloid leukemia (CML) from a life… 
Review
2010
Review
2010
Thiol-click chemistry: a multifaceted toolbox for small molecule and polymer synthesis.
The merits of thiol-click chemistry and its potential for making new forays into chemical synthesis and materials applications… 
Review
2008
Review
2008
Classification and diagnosis of myeloproliferative neoplasms: The 2008 World Health Organization criteria and point-of-care diagnostic algorithms
The 2001 World Health Organization (WHO) treatise on the classification of hematopoietic tumors lists chronic myeloproliferative… 
Highly Cited
2007
Highly Cited
2007
Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia.
Mutations in the kinase domain (KD) of BCR-ABL are the most prevalent mechanism of acquired imatinib resistance in patients with… 
Highly Cited
2005
Highly Cited
2005
Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl.
Highly Cited
2004
Highly Cited
2004
Overriding Imatinib Resistance with a Novel ABL Kinase Inhibitor
Resistance to the ABL kinase inhibitor imatinib (STI571 or Gleevec) in chronic myeloid leukemia (CML) occurs through selection… 
Highly Cited
2003
Highly Cited
2003
Structural Basis for the Autoinhibition of c-Abl Tyrosine Kinase
Highly Cited
2002
Highly Cited
2002
High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who…
Point mutations were found in the adenosine triphosphate (ATP) binding region of BCR/ABL in 12 of 18 patients with chronic… 
Highly Cited
2001
Highly Cited
2001
Crystal structures of the kinase domain of c-Abl in complex with the small molecule inhibitors PD173955 and imatinib (STI-571).
The inadvertent fusion of the bcr gene with the abl gene results in a constitutively active tyrosine kinase (Bcr-Abl) that… 
Review
2000
Review
2000
The molecular biology of chronic myeloid leukemia.
Chronic myeloid leukemia (CML) is probably the most extensively studied human malignancy. The discovery of the Philadelphia (Ph… 
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