PDF Mouse Monoclonal Antibody [Clone ID: OTI3C12]

CAT#: TA502989

PDF mouse monoclonal antibody, clone OTI3C12 (formerly 3C12)

Size: 30 ul 100 ul

Formulation: Standard Carrier-Free

Conjugation: Unconjugated Biotin HRP


  View other "OTI3C12" antibodies (4)

USD 447.00

In Stock*

Size
    • 100 ul

Frequently bought together (2)
Transient overexpression lysate of peptide deformylase (mitochondrial) (PDF), nuclear gene encoding mitochondrial protein
    • 100 ug

USD 436.00


beta Actin Mouse Monoclonal Antibody, Clone OTI1, Loading Control
    • 30 ul

USD 200.00

Specifications

Product Data
Clone Name OTI3C12
Applications FC, IF, WB
Recommended Dilution WB 1:500, IF 1:100, FLOW 1:100
Reactivities Human
Host Mouse
Isotype IgG1
Clonality Monoclonal
Immunogen Full length human recombinant protein of human PDF (NP_071736) produced in HEK293T cell.
Formulation PBS (pH 7.3) containing 1% BSA, 50% glycerol and 0.02% sodium azide.
Concentration 1 mg/ml
Purification Purified from mouse ascites fluids or tissue culture supernatant by affinity chromatography (protein A/G)
Conjugation Unconjugated
Storage Store at -20°C as received.
Stability Stable for 12 months from date of receipt.
Predicted Protein Size 19.4 kDa
Gene Name peptide deformylase, mitochondrial
Background Protein synthesis proceeds after formylation of methionine by methionyl-tRNA formyl transferase (FMT) and transfer of the charged initiator f-met tRNA to the ribosome. In eubacteria and eukaryotic organelles the product of this gene, peptide deformylase (PDF), removes the formyl group from the initiating methionine of nascent peptides. In eubacteria, deformylation of nascent peptides is required for subsequent cleavage of initiating methionines by methionine aminopeptidase. The discovery that a natural inhibitor of PDF, actinonin, acts as an antimicrobial agent in some bacteria has spurred intensive research into the design of bacterial-specific PDF inhibitors. In human cells, only mitochondrial proteins have N-formylation of initiating methionines. Protein inhibitors of PDF or siRNAs of PDF block the growth of cancer cell lines but have no effect on normal cell growth. In humans, PDF function may therefore be restricted to rapidly growing cells. [provided by RefSeq]
Reference Data

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