BACKGROUND HIV-1 Tat plays a pivotal role in both the HIV-1 replication cycle and in the pathogenesis of HIV-1 infection. Tat affects the HIV-1 replication cycle regulation by increasing proviral transcription rate several hundred-fold and acting on the elongation of viral transcripts. Moreover, Tat displays several important biological activities committed to uninfected and infected cells by a paracrine/autocrine mechanism due to secretion of Tat from infected cells. In particular, Tat modulates the expression of several cellular genes and triggers the activation of signal transduction pathways and transcription factors that suggest an important role in HIV-1 infection.1,2 A HIV Tat-derived peptide (RKKRRQRRR) has enabled the intracellular delivery of cargos of various sizes and physicochemical properties, including small particles, proteins, peptides, and nucleic acids.3 RECENT PUBLICATIONS Abudara, V., J. Bechberger, M. Freitas-Andrade, M. De Bock., N. Wang, G. Bultynck, C. Naus, L. Leybaert, and C. Giaume. 2014. The connexin43 mimetic peptide Gap19 inhibits hemichannels without altering gap junctional communication in astrocytes. Front Cell Neurosci, 8:306.
REFERENCES 1. Harrich, D., Curr Drug Targets. 7:1595, 2006. Products are for research use only. They are not intended for human, animal, or diagnostic applications. Параметры
*Optimal working dilutions must be determined by end user. Публикации
2014
Abudara, V., J. Bechberger, M. Freitas-Andrade, M. De Bock., N. Wang, G. Bultynck, C. Naus, L. Leybaert, and C. Giaume. 2014. The connexin43 mimetic peptide Gap19 inhibits hemichannels without altering gap junctional communication in astrocytes. Front Cell Neurosci, 8:306.
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