Results 121 to 130 of about 3,597,789 (164)
ObjectiveTo observe the effect of electroacupuncture (EA) at “Gongsun” (SP4) on tumor suppressor protein 53 (P53)/cyclin-dependent inhibitor 21 (P21) pathway in rats with premature ovarian insufficiency (POI), so as to investigate its underlying ...
ZHANG Dan-ni +4 more
doaj
Expression of the cyclin-dependent kinase inhibitor p16 during the ongoing cell cycle [PDF]
It has been demonstrated that protein expression of p16, the inhibitor of cyclin-dependent kinase 4 and 6, increases 4 fold at the G1/S transition when serum-arrested cells are restimulated to logarithmic growth.
Thomas Soucek +2 more
exaly +5 more sources
Homozygous loss of the cyclin-dependent kinase 4-inhibitor (p16) gene in human leukemias [PDF]
Abstract Recently, it has been shown that the homozygous deletion of the cyclin- dependent kinase-4 inhibitor (CDK4I;p16) gene, which is mapped to chromosome 9p21, is frequently observed in a wide spectrum of human cancers, including leukemias. Therefore, the CDK4I gene is thought to be a putative tumor-suppressor gene.
Kinuko Mitani, Naoto Hirano, A Hangaishi
exaly +5 more sources
Both p16 and p21 Families of Cyclin-dependent Kinase (CDK) Inhibitors Block the Phosphorylation of Cyclin-dependent Kinases by the CDK-activating Kinase * [PDF]
Phosphorylation of cyclin-dependent kinases (CDKs) by the CDK-activating kinase is required for the activation of CDK enzymes. Members of two families of CDK inhibitors, p16/p18 and p21/p27, become physically associated with and inhibit the activity of CDKs in response to a variety of growth-modulating signals.
Yue Xiong, Edison T Liu, E T Liu
exaly +3 more sources
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Expression of the cyclin-dependent kinase inhibitor p16 in Alzheimerʼs disease
NeuroReport, 1996Recent evidence indicates that an impairment of neuronal adaptive and reparative processes might be a key feature of the pathomechanism of Alzheimer's disease. Aberrations in the reparative neuronal response are likely to result from alterations of intracellular signal transduction cascades.
T, Arendt +3 more
openaire +2 more sources
British Journal of Haematology, 1995
Summary The cyclin‐dependent kinase inhibitors known as p15, p16 and p18 have been suggested as candidates for tumour suppressor genes. We examined these genes for their alterations in 46 myeloid leukaemias and 15 myeloid leukaemia cell lines, p16 mRNA expression was studied in 41 myeloid leukaemias. The p15 and p16 genes were either deleted or mutated
Juerg Schwaller +2 more
exaly +3 more sources
Summary The cyclin‐dependent kinase inhibitors known as p15, p16 and p18 have been suggested as candidates for tumour suppressor genes. We examined these genes for their alterations in 46 myeloid leukaemias and 15 myeloid leukaemia cell lines, p16 mRNA expression was studied in 41 myeloid leukaemias. The p15 and p16 genes were either deleted or mutated
Juerg Schwaller +2 more
exaly +3 more sources
Leukemia and Lymphoma, 1996
Neoplastic diseases are proliferative disorders characterized by uncoordinated cell growth. Cellular proliferation follows an orderly progression through the cell cycle, which is governed by different cyclins and cyclin dependent kinases (CDKs). Recently, CDK-inhibitors, which are a new class of small proteins involved in the negative regulation of the
Bertram Opalka, B Opalka, R Siebert
exaly +3 more sources
Neoplastic diseases are proliferative disorders characterized by uncoordinated cell growth. Cellular proliferation follows an orderly progression through the cell cycle, which is governed by different cyclins and cyclin dependent kinases (CDKs). Recently, CDK-inhibitors, which are a new class of small proteins involved in the negative regulation of the
Bertram Opalka, B Opalka, R Siebert
exaly +3 more sources
Searching for selective cyclin-dependent kinase inhibitors to target the retinoblastoma/p16 cancer gene pathway. [PDF]
Frédéric J Kaye
exaly +2 more sources
Receptor-Ck regulates the expression of cyclin-dependent kinase inhibitors (p16; p27)
Molecular and Cellular Biochemistry, 1999The present study was addressed to understand the interrelationship between Receptor-Ck induction-activation coupling; isoprenoids (derived from mevalonate pathway) and cyclin-dependent kinase inhibitors. The results reported here unambiguously reveal that isoprenoids regulate the expression of genes coding for CDK inhibited p16 and p27.
D, Kaul, M, Kaur
openaire +2 more sources

