Maf1 Polyclonal Antibody, 100ul Cell Transfection Mutations in OCRL cause oculocerebrorenal

Mutations in OCRL cause oculocerebrorenal syndrome of Lowe and also Dent disease

DUSP14 contains the consensus DUSP C-terminal catalytic domain but lacks the N-terminal CH2 domain found in the MKP (mitogen-activated protein kinase phosphatase) class of DUSPs (see MIM 600714) (summary by Patterson et al

and thus may regulate sodium channels by altering tyrosine phosphorylation status

Interacts with KRT17 (By similarity)

a circulating inhibitor of the formation of new blood vessels (angiogenesis)

Maf1 Polyclonal Antibody, 100ul Cell Transfection Mutations in OCRL cause oculocerebrorenalMAF1 (MAF1 homolog, negative regulator of RNA polymerase III) encodes a protein that is similar to Maf1, a Saccharomyces cerevisiae protein highly conserved in eukaryotic cells. Yeast Maf1 is a negative effector of RNA polymerase III (Pol III). It responds to changes in the cellular environment and represses pol III transcription. Biochemical studies identified the initiation factor TFIIIB as a target for Maf1 dependent repression.