Dr. Andrew J Paterson MD
Orthopedist | Orthopaedic Surgery of the Spine
Msc 10 5600 1 University Of New Albuquerque NM, 87131Rating
5/5
About
Dr. Andrew Paterson is an orthopaedic surgeon practicing in Albuquerque, NM. Dr. Paterson specializes in the diagnosis, treatment and rehabilitation of injuries, diseases and disorders of the bodys musculoskeletal system. As an orthopaedic surgeon, Dr. Paterson tends to bones, ligaments, muscles, joints, nerves and tendons. Orthopaedic surgeons can specialize in certain areas like the hand, spine, hip, foot and ankle, shoulder and elbow or the knee.
Education and Training
Univ of Louisville Sch of Med, Louisville Ky 1999
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Formyl-Met-Leu-Phe induces calcium-dependent tyrosine phosphorylation of Rel-1 in neutrophils.
- O-GlcNAc modification is an endogenous inhibitor of the proteasome.
- Phosphorylation of mouse glutamine-fructose-6-phosphate amidotransferase 2 (GFAT2) by cAMP-dependent protein kinase increases the enzyme activity.
- Accumulation of protein O-GlcNAc modification inhibits proteasomes in the brain and coincides with neuronal apoptosis in brain areas with high O-GlcNAc metabolism.
- Induction of KLF4 in basal keratinocytes blocks the proliferation-differentiation switch and initiates squamous epithelial dysplasia.
- Proteolytic processing of TGFalpha redirects its mitogenic activity: the membrane-anchored form is autocrine, the secreted form is paracrine.
- The histone acetyltransferase NCOAT contains a zinc finger-like motif involved in substrate recognition.
- Streptozotocin inhibits O-GlcNAcase via the production of a transition state analog.
- Location and characterization of the O-GlcNAcase active site.
- O-GlcNAc integrates the proteasome and transcriptome to regulate nuclear hormone receptors.
- Proteasome function is regulated by cyclic AMP-dependent protein kinase through phosphorylation of Rpt6.
- Metabolic control of proteasome function.
- Protein O-GlcNAcylation: a new signaling paradigm for the cardiovascular system.
- Thiazolidinediones mimic glucose starvation in facilitating Sp1 degradation through the up-regulation of beta-transducin repeat-containing protein.
- Increased O-GlcNAc causes disrupted lens fiber cell differentiation and cataracts.
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