Sulfation is a common modification of endogenous (lipids, proteins, and carbohydrates) and exogenous (xenobiotics and drugs) compounds. In mammals, the sulfate source is 3'-phosphoadenosine 5'-phosphosulfate (PAPS), created from ATP and inorganic sulfate. Two different tissue isoforms encoded by different genes synthesize PAPS. This gene encodes one of the two PAPS synthetases. Defects in this gene cause the Pakistani type of spondyloepimetaphyseal dysplasia. Two alternatively spliced transcript variants that encode different isoforms have been described for this gene.
A synthesized peptide derived from human PAQR8.
A synthesized peptide derived from human PAR4, corresponding to a region within C-terminal amino acids.
A synthesized peptide derived from human PAR4, corresponding to a region within N-terminal amino acids.
A synthesized peptide derived from human PAR4, corresponding to a region within the internal amino acids.
A synthesized peptide derived from human Parathyroid Hormone, corresponding to a region within the internal amino acids.
A synthesized peptide derived from human PARD3, corresponding to a region within C-terminal amino acids.
A synthesized peptide derived from human PARD3B.
This gene encodes a member of the PARD protein family. PARD family members interact with other PARD family members and other proteins; they affect asymmetrical cell division and direct polarized cell growth. Multiple alternatively spliced transcript variants have been described for this gene.PARD3 (Par-3 Family Cell Polarity Regulator) is a Protein Coding gene. Diseases associated with PARD3 include Gamma Heavy Chain Disease and Enamel Caries. Among its related pathways are Transcriptional activity of SMAD2/SMAD3-SMAD4 heterotrimer and Ras signaling pathway. GO annotations related to this gene include protein phosphatase binding and phosphatidylinositol-4,5-bisphosphate binding. An important paralog of this gene is PARD3B.
A synthesized peptide derived from human PARD6A, corresponding to a region within N-terminal amino acids.
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