Product Description
DMP1 Antibody | 60-228 | ProSci
Host: Rabbit
Reactivity: Human
Homology: N/A
Immunogen: This DMP1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 146-175 amino acids from the N-terminal region of human DMP1.
Research Area: Cell Cycle, Signal Transduction
Tested Application: WB
Application: For WB starting dilution is: 1:1000
Specificiy: N/A
Positive Control 1: N/A
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: 56 kDa
Validation: N/A
Isoform: N/A
Purification: This antibody is purified through a protein A column, followed by peptide affinity purification.
Clonality: Polyclonal
Clone: N/A
Isotype: Rabbit Ig
Conjugate: Unconjugated
Physical State: Liquid
Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.
Concentration: batch dependent
Storage Condition: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Alternate Name: Dentin matrix acidic phosphoprotein 1, DMP-1, Dentin matrix protein 1, DMP1
User Note: Optimal dilutions for each application to be determined by the researcher.
BACKGROUND: Dentin matrix acidic phosphoprotein is an extracellular matrix protein and a member of the small integrin binding ligand N-linked glycoprotein family. This protein, which is critical for proper mineralization of bone and dentin, is present in diverse cells of bone and tooth tissues. The protein contains a large number of acidic domains, multiple phosphorylation sites, a functional arg-gly-asp cell attachment sequence, and a DNA binding domain. In undifferentiated osteoblasts it is primarily a nuclear protein that regulates the expression of osteoblast-specific genes. During osteoblast maturation the protein becomes phosphorylated and is exported to the extracellular matrix, where it orchestrates mineralized matrix formation. Mutations in the gene are known to cause autosomal recessive hypophosphatemia, a disease that manifests as rickets and osteomalacia. The gene structure is conserved in mammals. Two transcript variants encoding different isoforms have been described for this gene.