scholarly journals Phosphorylation and Activation of Cell Division Cycle Associated 8 by Aurora Kinase B Plays a Significant Role in Human Lung Carcinogenesis

2007 ◽  
Vol 67 (9) ◽  
pp. 4113-4122 ◽  
Author(s):  
Satoshi Hayama ◽  
Yataro Daigo ◽  
Takumi Yamabuki ◽  
Daizaburo Hirata ◽  
Tatsuya Kato ◽  
...  
Keyword(s):  
Cell Division ◽  
Significant Role ◽  
Human Lung ◽  
Aurora Kinase ◽  
Cell Division Cycle ◽  
Lung Carcinogenesis ◽  
Aurora Kinase B

scholarly journals A CLK1-KKT2 Signaling Pathway Regulating Kinetochore Assembly in Trypanosoma brucei

mBio ◽  
2021 ◽  
Author(s):  
Manuel Saldivia ◽  
Adam J. M. Wollman ◽  
Juliana B. T. Carnielli ◽  
Nathaniel G. Jones ◽  
Mark C. Leake ◽  
...  
Keyword(s):  
Cell Division ◽  
Trypanosoma Brucei ◽  
Protein Complexes ◽  
Genomic Stability ◽  
Aurora Kinase ◽  
Eukaryotic Cells ◽  
Large Protein ◽  
Aurora Kinase B ◽  
Kinetochore Assembly ◽  
Dynamic Microtubule

In eukaryotic cells, kinetochores are large protein complexes that link chromosomes to dynamic microtubule tips, ensuring proper segregation and genomic stability during cell division. Several proteins tightly coordinate kinetochore functions, including the protein kinase aurora kinase B.

Regulation of genes for the cdc25 phosphatases is important for checkpoint control during the cell division cycle

2001 ◽  
Vol 120 (5) ◽  
pp. A501-A501
Author(s):  
U HAUGWITZ ◽  
M WIEDMANN ◽  
K SPIESBACH ◽  
K ENGELAND ◽  
J MOSSNER
Keyword(s):  
Cell Division ◽  
Cell Division Cycle ◽  
Checkpoint Control

scholarly journals Inhibition of Aurora Kinase B activity disrupts development and differentiation of salivary glands

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Abeer K. Shaalan ◽  
Tathyane H. N. Teshima ◽  
Abigail S. Tucker ◽  
Gordon B. Proctor
Keyword(s):  
Cell Cycle ◽  
Embryonic Development ◽  
Salivary Glands ◽  
Aurora Kinase ◽  
Serine Threonine Kinase ◽  
Aurora Kinase B ◽  
Development And Differentiation ◽  
Differentiation Marker ◽  
Key Events

AbstractLittle is known about the key molecules that regulate cell division during organogenesis. Here we determine the role of the cell cycle promoter aurora kinase B (AURKB) during development, using embryonic salivary glands (E-SGs) as a model. AURKB is a serine/threonine kinase that regulates key events in mitosis, which makes it an attractive target for tailored anticancer therapy. Many reports have elaborated on the role of AURKB in neoplasia and cancer; however, no previous study has shown its role during organ development. Our previous experiments have highlighted the essential requirement for AURKB during adult exocrine regeneration. To investigate if AURKB is similarly required for progression during embryonic development, we pharmacologically inhibited AURKB in developing submandibular glands (SMGs) at embryonic day (E)13.5 and E16.5, using the highly potent and selective drug Barasertib. Inhibition of AURKB interfered with the expansion of the embryonic buds. Interestingly, this effect on SMG development was also seen when the mature explants (E16.5) were incubated for 24 h with another cell cycle inhibitor Aphidicolin. Barasertib prompted apoptosis, DNA damage and senescence, the markers of which (cleaved caspase 3, γH2AX, SA-βgal and p21, respectively), were predominantly seen in the developing buds. In addition to a reduction in cell cycling and proliferation of the epithelial cells in response to AURKB inhibition, Barasertib treatment led to an excessive generation of reactive oxygen species (ROS) that resulted in downregulation of the acinar differentiation marker Mist1. Importantly, inhibition of ROS was able to rescue this loss of identity, with Mist1 expression maintained despite loss of AURKB. Together, these data identify AURKB as a key molecule in supporting embryonic development and differentiation, while inhibiting senescence-inducing signals during organogenesis.

scholarly journals A Molecular Modeling Approach to Identify Potential Antileishmanial Compounds Against the Cell Division Cycle (cdc)-2-Related Kinase 12 (CRK12) Receptor of Leishmania donovani

Biomolecules ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 458
Author(s):  
Emmanuel Broni ◽  
Samuel K. Kwofie ◽  
Seth O. Asiedu ◽  
Whelton A. Miller ◽  
Michael D. Wilson
Keyword(s):  
Natural Products ◽  
Cell Division ◽  
Leishmania Donovani ◽  
Therapeutic Potential ◽  
Neglected Tropical Diseases ◽  
Binding Pocket ◽  
Cell Division Cycle ◽  
World Health ◽  
Atp Binding ◽  
African Flora

The huge burden of leishmaniasis caused by the trypanosomatid protozoan parasite Leishmania is well known. This illness was included in the list of neglected tropical diseases targeted for elimination by the World Health Organization. However, the increasing evidence of resistance to existing antimonial drugs has made the eradication of the disease difficult to achieve, thus warranting the search for new drug targets. We report here studies that used computational methods to identify inhibitors of receptors from natural products. The cell division cycle-2-related kinase 12 (CRK12) receptor is a plausible drug target against Leishmania donovani. This study modelled the 3D molecular structure of the L. donovani CRK12 (LdCRK12) and screened for small molecules with potential inhibitory activity from African flora. An integrated library of 7722 African natural product-derived compounds and known inhibitors were screened against the LdCRK12 using AutoDock Vina after performing energy minimization with GROMACS 2018. Four natural products, namely sesamin (NANPDB1649), methyl ellagic acid (NANPDB1406), stylopine (NANPDB2581), and sennecicannabine (NANPDB6446) were found to be potential LdCRK12 inhibitory molecules. The molecular docking studies revealed two compounds NANPDB1406 and NANPDB2581 with binding affinities of −9.5 and −9.2 kcal/mol, respectively, against LdCRK12 which were higher than those of the known inhibitors and drugs, including GSK3186899, amphotericin B, miltefosine, and paromomycin. All the four compounds were predicted to have inhibitory constant (Ki) values ranging from 0.108 to 0.587 μM. NANPDB2581, NANPDB1649 and NANPDB1406 were also predicted as antileishmanial with Pa and Pi values of 0.415 and 0.043, 0.391 and 0.052, and 0.351 and 0.071, respectively. Molecular dynamics simulations coupled with molecular mechanics Poisson–Boltzmann surface area (MM/PBSA) computations reinforced their good binding mechanisms. Most compounds were observed to bind in the ATP binding pocket of the kinase domain. Lys488 was predicted as a key residue critical for ligand binding in the ATP binding pocket of the LdCRK12. The molecules were pharmacologically profiled as druglike with inconsequential toxicity. The identified molecules have scaffolds that could form the backbone for fragment-based drug design of novel leishmanicides but warrant further studies to evaluate their therapeutic potential.

scholarly journals RNA-binding protein RNPC1 acts as an oncogene in gastric cancer by stabilizing Aurora kinase B mRNA

2021 ◽  
pp. 112741
Author(s):  
Chun-Mei Ji ◽  
Xu Zhang ◽  
Wentong Fang ◽  
Ling Meng ◽  
Xiaolong Wei ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Aurora Kinase ◽  
Aurora Kinase B

scholarly journals Targeting Cell Division Cycle 25 Homolog B To Regulate Influenza Virus Replication

2013 ◽  
Vol 87 (24) ◽  
pp. 13775-13784 ◽  
Author(s):  
O. Perwitasari ◽  
A. C. Torrecilhas ◽  
X. Yan ◽  
S. Johnson ◽  
C. White ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Cell Division ◽  
Virus Replication ◽  
Cell Division Cycle ◽  
Influenza Virus Replication

scholarly journals Aurora Kinase B Inhibition: A Potential Therapeutic Strategy for Cancer

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 1981
Author(s):  
Naheed Arfin Borah ◽  
Mamatha M. Reddy
Keyword(s):  
Drug Resistance ◽  
Cell Cycle Progression ◽  
Therapeutic Strategy ◽  
Tumor Development ◽  
Aurora Kinase ◽  
Aurora Kinase B ◽  
Development Therapy ◽  
Chromosomal Passenger ◽  
Combination Studies ◽  
Related Drug

Aurora kinase B (AURKB) is a mitotic serine/threonine protein kinase that belongs to the aurora kinase family along with aurora kinase A (AURKA) and aurora kinase C (AURKC). AURKB is a member of the chromosomal passenger protein complex and plays a role in cell cycle progression. Deregulation of AURKB is observed in several tumors and its overexpression is frequently linked to tumor cell invasion, metastasis and drug resistance. AURKB has emerged as an attractive drug target leading to the development of small molecule inhibitors. This review summarizes recent findings pertaining to the role of AURKB in tumor development, therapy related drug resistance, and its inhibition as a potential therapeutic strategy for cancer. We discuss AURKB inhibitors that are in preclinical and clinical development and combination studies of AURKB inhibition with other therapeutic strategies.

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