Dr. Boris M. Peterlin MD
Rheumatologist | Rheumatology
400 Parnassus Ave 405 Irving Street San Francisco CA, 94143About
Dr. Boris Peterlin is a rheumatologist practicing in San Francisco, CA. Dr. Peterlin specializes in the treatment of musculoskeletal diseases and systematic autoimmune conditions that can affect the bones, muscles or bones. Eventually, if not treated, these illnesses can also impact the skin, eyes, nervous system and internal organs. Dr. Peterlin treats diseases similar to orthopedists but does not perform surgery. Often times, research is conducted to find potential alternatives for the patients illness.
Education and Training
Harvard Medical School 1973
Board Certification
Internal MedicineAmerican Board of Internal MedicineABIM- Rheumatology
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Activation of Ste20 by Nef from human immunodeficiency virus induces cytoskeletal rearrangements and downstream effector functions in Saccharomyces cerevisiae.
- Activation of Vav by Nef induces cytoskeletal rearrangements and downstream effector functions.
- Tat transactivation: a model for the regulation of eukaryotic transcriptional elongation.
- The class II transactivator CIITA is a transcriptional integrator.
- Interactions between equine cyclin T1, Tat, and TAR are disrupted by a leucine-to-valine substitution found in human cyclin T1.
- Tat competes with CIITA for the binding to P-TEFb and blocks the expression of MHC class II genes in HIV infection.
- HIV-1 replication is inhibited by a pseudo-substrate peptide that blocks Tat transactivation.
- Mutation of a conserved residue (D123) required for oligomerization of human immunodeficiency virus type 1 Nef protein abolishes interaction with human thioesterase and results in impairment of Nef biological functions.
- Mutations in the bare lymphocyte syndrome define critical steps in the assembly of the regulatory factor X complex.
- Binding of Tat to TAR and recruitment of positive transcription elongation factor b occur independently in bovine immunodeficiency virus.
- Inhibition of the RNA-dependent transactivation and replication of human immunodeficiency virus type 1 by a fluoroquinoline derivative K-37.
- Flavopiridol inhibits P-TEFb and blocks HIV-1 replication.
- Endocytic entry of HIV-1.
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