Información del producto
CDK9 antibody
Información adicional
Size
100µg
Storage Conditions
PBS with 0.02% sodium azide and 50% glycerol pH 7.3, -20℃ for 12 months(Avoid repeated freeze / thaw cycles.)
Applications
ELISA, WB, IHC
Target
CDK9
Research Area
Cell Division and Proliferation, Metabolism
Form
liquid
Recomended Dilution
IHC: 1:20-1:200
WB: 1:500-1:2000
WB: 1:500-1:2000
Type Clonality
polyclonal
Immunogen
cyclin-dependent kinase 9
Minimum Purity
≥95% as determined by SDS-PAGE
Synonyms
Cyclin-dependent kinase 9|C-2K|Cell division cycle 2-like protein kinase 4|Cell division protein kinase 9|Serine/threonine-protein kinase PITALRE|Tat-associated kinase complex catalytic subunit|CDK9|CDC2L4|TAK
Host
Rabbit
UniProt ID
P50750
Gene ID
1025
Purification
Immunogen affinity purified
Iso type
IgG
Reactivity
Human, Mouse, Rat
Observed MW
43 kDa
Background
Protein kinase involved in the regulation of transcription. Member of the cyclin-dependent kinase pair(CDK9/cyclin-T) complex, also called positive transcription elongation factor b(P-TEFb), which facilitates the transition from abortive to productive elo
integrates phosphorylation during transcription with chromatin modifications to control co-transcriptional histone mRNA processing. The CDK9/cyclin-K complex has also a kinase activity towards CTD of RNAP II and can substitute for CDK9/cyclin-T P-TEFb in
the CDK9/cyclin-K complex is required for genome integrity maintenance, by promoting cell cycle recovery from replication arrest and limiting single-stranded DNA amount in response to replication stress, thus reducing the breakdown of stalled replication
integrates phosphorylation during transcription with chromatin modifications to control co-transcriptional histone mRNA processing. The CDK9/cyclin-K complex has also a kinase activity towards CTD of RNAP II and can substitute for CDK9/cyclin-T P-TEFb in
the CDK9/cyclin-K complex is required for genome integrity maintenance, by promoting cell cycle recovery from replication arrest and limiting single-stranded DNA amount in response to replication stress, thus reducing the breakdown of stalled replication