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he results support the concept that P19ink4d may play an important role in the pathogenesis and development of noise induced hearing loss.
p19(INK4d) plays an active role during human tooth development along with MSX1 and MSX2
We unexpectedly found that p19INK4d plays an important role in human terminal erythropoiesis
p19(INK4D) is one of the key mediators of miR-125b activity during the onset of megakaryocyte polyploidization.
p19 may play an important role in the ototoxic effects of cisplatin and is probably involved in the pathogenesis of hearing loss.
MiR-451 inhibited the proliferation of esophageal squamous cell carcinoma cells by targeting CDKN2D and MAP3K1 expression.
Data indicate that upon oxidative DNA damage, cyclin-dependent kinase inhibitor p19INK4d strongly binds to and relaxes chromatin.
CDKN2D repression by PML/RARalpha disrupts both cell proliferation and differentiation in the pathogenesis of acute promyelocytic leukemia.
p19-INK4d inhibits neuroblastoma cell growth, induces differentiation and is hypermethylated and downregulated in MYCN-amplified neuroblastomas.
CDKN2D-WDFY2 fusion could be an important molecular signature for understanding and classifying sub-lineages among heterogeneous high-grade serous ovarian carcinomas.
Mutations in CDKN2D is associated with sporadic parathyroid adenoma.
P19(INK4d) expression is a poor prognostic factor in ovarian cancer patients.
PTB plays as a negative regulator in H1299 cell proliferation at least by inducing p19(Ink4d) expression at transcriptional and post-transcriptional levels.
Up-regulation of CDKN2D during in-vitro passages of human amniotic fluid-derived mesenchymal stromal cells may indicate the begging of early senescence process in a p53-independent mechanism.
E2F1 is involved in the induction of p19INK4d following UV irradiation
CDK2 and PKA mediated-sequential phosphorylation is critical for p19INK4d function in the DNA damage response to ensure cell survival.
expression of p19INK4D may be an effective predictor of clinical behavior in hepatocellular carcinoma, and therefore, a new prognostic marker
p19INK4d is transcriptionally regulated by E2F1 through two response elements present in the p19INK4d promoter.
protein folding and stability
The human p19(INK4d) gene is under the control of TATA-less promoter and the Sp1 binding site is involved in the transcription.
The expression of three tumor suppressor genes encoded in the INK4/ARF locus (p15(INK4b), p16(INK4a), and p19(ARF)) was decreased in E6AP(-/-) embryo fibroblasts.
TWIST1-E protein heterodimeric complexes may thus constitute the main active forms of TWIST1 with regard to senescence inhibition over the time course of breast tumorigenesis.
Rescue from early-onset hearing loss in a mouse model lacking the cyclin-dependent kinase inhibitor p19Ink4d.
p19 INK4d controls hematopoietic stem cells in a cell-autonomous manner during genotoxic stress and through the microenvironment during aging
Cdk4 and Cdk6 cooperate in hematopoietic tumor development and suggest a role for Cdk6 in sequestering INK4 proteins away from Cdk4.
Deletion of p19(Ink4d) (p19), a cyclin-dependent kinase CDK inhibitor gene, in mice results in spontaneous development of tumors in multiple organs and tissues.
We propose that p19INK4d participates in the cellular mechanisms that trigger senescence by contributing to chromatin compaction
CDK5-mediated phosphorylation of p19INK4d avoids DNA damage-induced neurodegeneration in mouse hippocampus and prevents loss of cognitive functions.
an asymmetrical distribution pattern for Cdkn2d transcripts in 2-cell embryos.
Ectopic expression of RUVBL2 decreases the levels of ARF, whereas knockdown of RUVBL2 results in a marked increase in ARF levels. In addition, RUVBL2 down-regulates the levels of p53 in an ARF-dependent manner.
DeltaNp63alpha has oncogenic activity and its overexpression in human squamous cell carcinomas contributes to the malignant phenotype, and implicate its ability to regulate p16(ink4a)/p19(arf) in the process.
A significant proportion of immortalised cell cultures apparently had neither a p53 mutation nor loss of p19/ARF.
The cyclin-dependent kinase inhibitors p19(Ink4d) and p27(Kip1) are coexpressed in select retinal cells and act cooperatively to control cell cycle exit.
Deletion of Ink4d alone is sufficient to disrupt the maintenance of the post-mitotic state of sensory hair cells in post-natal mice. In Ink4d-/- animals, hair cells re-enter the cell cycle and undergo apoptosis, resulting in progressive hearing loss.
Cranial neural crest-derived mesenchymal proliferation is regulated by Msx1-mediated p19(INK4d) expression during odontogenesis.
p19(Ink4d) & p21(Cip1) codeletion triggers S-phase entry of auditory hair cells in early postnatal life & transient appearance of supernumerary hair cells. Aberrant cell cycle reentry activates a DNA damage response pathway & p53-mediated apoptosis.
Results describe the expression of p18(Ink4c) and p19(Ink4d) in spermatogenic and supporting cells in the testis and in pituitary gonadotropes.
These studies indicate that a reduction in Ink4 family function by the loss of p19(Ink4d) is sufficient to induce mild reproductive defects in male mice with a mixed genetic background, but not in the C57BL/6 genetic background.
p19(INK4D) knockdown led to a moderate increase (31.7% +/- 5%) in the mean ploidy of megakaryocytes suggesting a role of p19(INK4D) in the endomitotic arrest.
p18Ink4c and p19Ink4d protein levels are not only differentially regulated by the ubiquitin-proteasome pathway, but are subject to completely opposite modes of regulation when associated with their target Cdks.
The protein encoded by this gene is a member of the INK4 family of cyclin-dependent kinase inhibitors. This protein has been shown to form a stable complex with CDK4 or CDK6, and prevent the activation of the CDK kinases, thus function as a cell growth regulator that controls cell cycle G1 progression. The abundance of the transcript of this gene was found to oscillate in a cell-cycle dependent manner with the lowest expression at mid G1 and a maximal expression during S phase. The negative regulation of the cell cycle involved in this protein was shown to participate in repressing neuronal proliferation, as well as spermatogenesis. Two alternatively spliced variants of this gene, which encode an identical protein, have been reported.
cyclin-dependent kinase inhibitor 2D (p19, inhibits CDK4)
, cyclin-dependent kinase 4 inhibitor D
, Cyclin-dependent kinase 4 inhibitor D
, CDK inhibitor p19INK4d
, cell cycle inhibitor, Nur77 associating protein
, cyclin-dependent kinase 4 inhibitor D p19
, inhibitor of cyclin-dependent kinase 4d