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ADP-ribosylation is a reversible posttranslational modification used to regulate protein function.
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Hybrid human-Xenopus Adprhl1 (zeige LGALS4 ELISA Kits)protein constructs were produced by utilizing restriction sites from one species and engineering the same site into the second species by PCR. Hearts containing human ADPRHL1 developed normally. Engineered human-Xenopus hybrid proteins cause extensive branching of myofibrils with sarcomere division occurring at the actin-Z-disc boundary.
Cardiac Adprhl1 expression is (zeige LGALS4 ELISA Kits) conserved in mammals, with Adprhl1 mRNA detected within embryonic mouse hearts at E11.5 and its expression may depend on the presence of the cardiac transcription factor, Nkx2-5.
Using a cardiac-specific Gal4 (zeige LGALS4 ELISA Kits) binary expression system, we show that the abundance of Adprhl1 protein in tadpole hearts is tightly controlled through a negative regulatory mechanism targeting the 5'-coding sequence of Xenopus adprhl1. Over-expression of full length (40kDa) Adprhl1 variants modified to escape such repression, also disrupts cardiac myofibrillogenesis.
ADP-ribosylation is a reversible posttranslational modification used to regulate protein function. ADP-ribosyltransferases (see ART1\; MIM 601625) transfer ADP-ribose from NAD+ to the target protein, and ADP-ribosylhydrolases, such as ADPRHL1, reverse the reaction (Glowacki et al., 2002
, ADP-ribosylhydrolase 2
, [Protein ADP-ribosylarginine] hydrolase-like protein 1