ccnd1

CCND1 Protein, Human, Recombinant (His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 37.7 kDa and the accession number is P24385.

RPRD1B, together with RPRD1A, can accompany RNAP II from promoter regions to 3'-untranslated regions during transcription in vivo, predominantly interact with phosphorylated RNAP II, and can reduce CTD S5- and S7-phosphorylated RNAP II at target gene promoters. RNA polymerase II C-terminal domain (CTD) phosphorylation is important for various transcription-related processes. RPRD1B is a transcriptional regulator that enhances expression of CCND1. It also enhances the transcription of a number of other cell cycle-related genes including CDK2, CDK4, CDK6 and cyclin-E but not CDKN1A, CDKN1B or cyclin-A.

ATOX1 is a cytoplasmic copper chaperone that interacts with the copper-binding domain of the membrane copper transporters ATP7A and ATP7B. ATOX1 has also been suggested to have a potential anti-oxidant activity. As the trace element copper is essential, but extremely toxic in high concentrations, intracellular copper concentrations are tightly controlled. Once in the cell, copper is distributed by metallochaperones, including the small cytoplasmic protein ATOX1. ATOX1 plays an important role in the transfer of copper to the copper export P-type ATPases ATP7A and ATP7B to facilitate copper excretion. There is a novel function for Atox1 as a transcription factor (TF) regulating Ccnd1 was proposed. Antioxidant 1 (ATOX1) functions as an antioxidant against hydrogen peroxide and superoxide, and therefore may play a significant role in many human diseases, including diabetes mellitus (DM). The transduced Tat-ATOX1 protein protects pancreatic beta-cells by inhibiting STZ-induced cellular toxicity in vitro and in vivo. Thus Tat-ATOX1 protein has potential applications as a therapeutic agent for oxidative stress-induced diseases including DM.

Possesses dinucleoside triphosphate hydrolase activity. Cleaves P(1)-P(3)-bis(5'-adenosyl) triphosphate (Ap3A) to yield AMP and ADP. Can also hydrolyze P(1)-P(4)-bis(5'-adenosyl) tetraphosphate (Ap4A), but has extremely low activity with ATP. Exhibits adenylylsulfatase activity, hydrolyzing adenosine 5'-phosphosulfate to yield AMP and sulfate. Exhibits adenosine 5'-monophosphoramidase activity, hydrolyzing purine nucleotide phosphoramidates with a single phosphate group such as adenosine 5'monophosphoramidate (AMP-NH2) to yield AMP and NH2. Exhibits adenylylsulfate-ammonia adenylyltransferase, catalyzing the ammonolysis of adenosine 5'-phosphosulfate resulting in the formation of adenosine 5'-phosphoramidate. Also catalyzes the ammonolysis of adenosine 5-phosphorofluoridate and diadenosine triphosphate. Modulates transcriptional activation by CTNNB1 and thereby contributes to regulate the expression of genes essential for cell proliferation and survival, such as CCND1 and BIRC5. Plays a role in the induction of apoptosis via SRC and AKT1 signaling pathways. Inhibits MDM2-mediated proteasomal degradation of p53/TP53 and thereby plays a role in p53/TP53-mediated apoptosis. Induction of apoptosis depends on the ability of FHIT to bind P(1)-P(3)-bis(5'-adenosyl) triphosphate or related compounds, but does not require its catalytic activity. Functions as tumor suppressor.

Cyclin-Dependent Kinase Inhibitor 1B (CDKN1B) is a Kinesin-related motor protein necessary for mitotic spindle assembly and chromosome segregation. CDKN1B is expressed in all tissues with highest levels observed in skeletal muscle. CDKN1B is a potent inhibitor of Cyclin E- and Cyclin A-CDK2 complexes. CDKN1B forms a complex with Cyclin Type D-CDK4 complexes and is involved in the assembly, stability, and modulation of CCND1-CDK4 complex activation. In addition, CDKN1B acts as an inhibitor or an activator of Cyclin Type D-CDK4 complexes depending on its phosphorylation state and stoichometry.