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The enzyme encoded by TYR catalyzes the first 2 steps, and at least 1 subsequent step, in the conversion of tyrosine to melanin. Additionally we are shipping Tyrosinase Antibodies (297) and Tyrosinase Kits (64) and many more products for this protein.
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Retinal pigment epithelium (which normally expresses tyrosinase) secretes a modulatory factor, possibly L-DOPA, which regulates light adaptation in the retinal circuitry.
Transcription of the tyrosinase gene family in an Atlantic salmon leukocyte cell line (SHK (show SHPK Proteins)-1) is influenced by temperature, but not by virus infection or bacterin stimulation.
The effect of histidine mutations on the structural stability of human tyrosinase leading to albinism has been reported.
Compound heterozygous mutations (c.832C>T and c.929_930insC) in the TYR gene may be responsible for partial clinical manifestations of oculocutaneous albinism
Mutations in tyrosinase gene is associated with Oculocutaneous albinism type 1.
tyrosinase as a potential GPR143 (show GPR143 Proteins) binding protein opens new avenues for investigating the mechanisms that regulate pigmentation and neurogenesis.
Aberrant tyrosinase expression in an atypical fibroxanthoma
Findings suggested that miR (show MLXIP Proteins)-330-5p represents a potential tumor-suppressive miRNA and plays an important role in cutaneous malignant melanoma progression by suppressing TYR and PDIA3 (show PDIA3 Proteins) expression.
Four missense substitutions (p.Arg239Trp, p.Ser192Tyr, p.Ser44Arg and p.Arg77Gln) were identified in tyrosinase in the families with oculocutaneous albinism linkage, and another missense substitution (p.Gln272Lys) was identified in the family with OCA4 linkage
LEF-1 (show LEF1 Proteins) and MITF (show MITF Proteins) regulate tyrosinase gene transcription in vitro via binding to its promoter.
Data show that mutant microphthalmia-associated transcription factor (MITF (show MITF Proteins)) with loss of localization signals (NLS (show ALDH1A2 Proteins)) has failed to transactivate the transcriptional activities of target gene tyrosinase (TYR), which can cause Waardenburg syndrome.
The tyrosinase gene was examined in 23 unrelated patients with autosomal recessive ocular albinism or nonsyndromic oculocutaneous albinism. TYR gene mutations were identi fi ed in 14 (app (show APP Proteins). 60%) albinism patients.
This study demonstrates the utility of CRISPR-Cas9 system in generating domain-specific in-frame deletions and helps gain further insights into structure-function of Tyr gene.
These results suggest that the tyrosinase-induced metabolism of rhodendrol causes melanocyte toxicity.
Data indicate that both ephedrannins A and B were competitive inhibitors of mushroom tyrosinase.
STAP-2 (show STAP2 Proteins) colocalized with tyrosinase in lysosomes and protected tyrosinase from protein degradation in B16F10 melanoma cells.
Docosahexaenoic acid inhibits melanogenesis in B16F10 cells in vitro through increased tyrosinase degradation.
Studied upregulation by Kaliziri extract of tyrosinase, TRP-1 (show TRPC1 Proteins), TRP-2 (show DCT Proteins) and MITF (show MITF Proteins) expression in murine B16 melanoma cells.
The albino mutation of tyrosinase alters ocular angiogenic responsiveness.
Tyrosinase is mutated in the albino dorsal lateral geniculate nucleus, arising from retinal ganglion cell misspecification together with potential perturbations of early activity patterns in the albino retina.
activated by ascorbic acid in B16 melanoma via p38 MAPK (show MAPK14 Proteins) signaling and upregulation of melanogenic regulatory factors
Effect of zibuganshenfang on the expression and activity of tyrosinase on B16 cells
we identified some genes that are related to fur formation, including Tyrosinase-related protein 1 (TYRP1 (show TYRP1 Proteins)) and Tyrosinase (TYR), as well as genes with unknown functions.
The enzyme encoded by this gene catalyzes the first 2 steps, and at least 1 subsequent step, in the conversion of tyrosine to melanin. The enzyme has both tyrosine hydroxylase and dopa oxidase catalytic activities, and requires copper for function. Mutations in this gene result in oculocutaneous albinism, and nonpathologic polymorphisms result in skin pigmentation variation. The human genome contains a pseudogene similar to the 3' half of this gene.
, hypothetical protein
, tyrosinase (oculocutaneous albinism IA)
, monophenol monooxygenase
, oculocutaneous albinism IA
, tumor rejection antigen AB
, albino locus protein