In the synthesis pathway for the catecholamines - dopamine, epinephrine, and norepinephrine, tyrosine hydroxylase is the rate-limiting enzyme. Through alternative mRNA splicing, a wide molecular diversity of TH isoforms are generated that are tissue-specific and carry varied enzymatic activities, allowing for differential neurotransmitter availability at various synapses. The devastating condition of Parkinson's disease (PD) is due to a TH deficiency, where dopaminergic neuron degeneration and low dopamine levels consistently are present, along with gross neurochemical abnormalities when monitored by tyrosine hydroxylase antibody staining1. Tyrosine hydroxylase antibody staining patterns in postmortem PD brain samples indicate that phosphorylation at the N-terminus of the TH molecule triggers global proteasomal degradation2. In those studies, the establishment of a needed transgenic knockout mouse model depended on successful tyrosine hydroxylase antibody verification of both clinical and neurochemical phenotypes. Results obtained with the tyrosine hydroxylase antibody were published in Cell, where researchers identified the parkin interacting substrate (PARIS/ZNF746), and demonstrated that it causes progressive classic PD dopamine neuron loss in a transcriptional co activator PGC-dependent manner3.
Immunocytochemistry/Immunofluorescence: Tyrosine Hydroxylase Antibody
Immunofluorescent and immunohistochemical studies on transgenic mice models were done by Lee’s group with the tyrosine hydroxylase antibody to show that brain-permeable PARP inhibitors were able to slow down PD behavioral deficits as well as dopamine neuron death4. Similar transgenic immunofluorescence and immunohistochemistry with the tyrosine hydroxylase antibody were also performed by Wei’s group to examine the role of supersensitive spiny neurons (D2-MSNs) as a compensatory mechanism for lost dopamine receptors5.
Novus Biologicals offers Tyrosine hydroxylase reagents for your research needs including:
