Figure 3

Transglutaminase inhibition: possible therapeutic mechanisms to protect cells from death in neurological disorders

Vittorio Gentile*, Elenamaria Fioretti, Nicola Gaetano Gatta and Rosaria Romano

Published: 25 July, 2017 | Volume 1 - Issue 1 | Pages: 026-038


Figure 3:

Possible physiopathological effects of the mutated huntingtin. Some of the physiopathological roles of mutated huntingtin, including the formation of nuclear inclusions, have been described in the Figure AP2=adipocyte Protein 2; BAX=bcl-2-like protein 4; BDNF=brain-derived neurotrophic factor; CALM= calmodulin; CASP=caspases; CASP3=caspase 3; CASP8=caspase 8; CBP= CREB binding protein; CBS = cystathionine-β-synthase; DCTN1 = dynactin subunit 1; GAPD=glyceraldehyde-3-phosphate dehydrogenase; GRB2=growth factor receptor-bound protein 2; HAP1=huntingtin associated protein 1; HIP1=huntingtin interacting protein 1; HIP2=huntingtin interacting protein 2; Hippi; HIP1 protein interactor; NCOR1=nuclear receptor corepressor 1; RasGAP=p21Ras protein and GTPase-activating protein complex; TGs=transglutaminases; TP53=tumor protein 53.

Read Full Article HTML DOI: 10.29328/journal.hjbm.1001004 Cite this Article Read Full Article PDF

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