Question: Which cyclin- dependent kinase inhibitor is regulated by Bmi-1?

Context:
the knockdown of BMI-1 expression could lead to significant up-regulation of p16INK4a
In EC9706 cells transfected by Bmi-1 siRNA, the expression levels of p16 
One important pathway regulated by Bmi-1 is that involving two cyclin-dependent kinase inhibitors, p16(Ink4a) and p19(Arf)
We also observe that ROS-induced up-regulation of p16(Ink4a) occurs correlatively with ERK1/2-dependent down-regulation and subsequent dissociation from chromatin of Bmi-1
Bmi-1 is important for postnatal, but not embryonic, neural stem cell (NSC) self-renewal and have identified the cell-cycle inhibitors p16/p19 as molecular targets
Bmi-1 function in stem cells during development that, surprisingly, seems to involve regulation of the cell-cycle inhibitor p21
Our data therefore implicate p21 as an important Bmi-1 target in NSCs
Bmi-1-mediated repression of Cdkn2A
decreased expression of proliferating cell nuclear antigen and Bmi-1; upregulation of p16(INK4a)
BMI-1 promotes self-renewal of stem cells largely by interfering with two central cellular tumor suppressor pathways, p16(Ink4a)
p16INK4a and p14ARF tumor suppressors, human telomerase reverse transcriptase (h-TERT), and oncoprotein c-Myc have been implicated in the regulation of the cell cycle and proliferation mediated by PcG proteins, mainly Bmi-1
involving the polycomb group repressor Bmi-1 and the cyclin-dependent kinase inhibitor p16(INK4a)
increased frequency to a telomere-independent senescent state mediated by the cyclin-dependent kinase inhibitor p16(INK4a). p16(INK4a) expression was regulated by the Polycomb group repressor Bmi-1
The antisense Bmi-1 gene can inhibit the growth of K562 cell and upgrade expression of p16 in K562 cells
overexpression of BMI-1, a transcriptional repressor of the p16(INK4a) locus,
experimental model systems indicate that p16 is a downstream target of Bmi
In the absence of Bmi-1, the cyclin-dependent kinase inhibitor gene p16Ink4a is upregulated in neural stem cells, reducing the rate of proliferation
A gene expression analysis revealed that the expression of stem cell associated genes, cell survival genes, transcription factors, and genes modulating proliferation including p16Ink4a and p19Arf was altered in bone marrow cells of the Bmi-1-/- mice
polycomb protein Bmi-1 represses the INK4a locus, which encodes the tumor suppressors p16 and p14(ARF)
Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus
in bmi-1-deficient lymphocytes, the expression of the tumour suppressors p16 and p19Arf, which are encoded by ink4a, is raised markedly
BMI-1-mediated INK4a/ARF pathway 
 expression of the polycomb protein BMI-1 and its downstream targets p16(Ink4a)
reduced expression of Bmi-1, OC, DSP, and BSP compared with rapidly proliferating cells, whereas p16(INK4A) level increased.
16Ink4a suppression of lung adenocarcinoma by Bmi-1
The suppression of p16Ink4a occurred in parallel with an increase in Bmi-1
Bmi-1 overexpression reduced p16(INK4a) promoter activity 
mi-1 regulates the Ink4a/Arf locus
derepression of the Ink4a/Arf locus is associated with decreased Bmi-1 binding,
pronounced effects of Bmi-1 over-expression in culture were largely attributable to the attenuated induction of p16(Ink4a) 
BMI-1 is a transcriptional repressor of the Ink4a/Arf locus encoding p16(ink4a)
introduction of Bmi-1 can inhibit p16(INK4a) expression
Bmi-1 promotes stem cell self-renewal partly by repressing the expression of Ink4a 
Overexpression of Bmi-1 in NPECs led to the induction of human telomerase reverse transcriptase activity and reduction of p16(INK4a) expression
Bmi-1 thus prevents the premature senescence of neural stem cells by repressing Ink4a
overexpression of the polycomb-group gene BMI-1 might also down-regulate p16 expression
Bmi-1 oncoprotein is overexpressed in human colorectal cancer and correlates with the reduced p16INK4a/p14ARF
modulation of Bmi-1 protein might be involved in human colorectal carcinogenesis by repressing the INK4a/ARF protein
mi-1 regulation of INK4A-ARF
expression of BMI-1, a lymphoid oncogene whose product functions as a transcriptional repressor of the INK4A-ARF tumor suppressor locu
bmi-1 oncoprotein is differentially expressed in non-small cell lung cancer and correlates with INK4A-ARF locus expression
bmi-1 overexpression induces immortalization due to repression of p16/p19ARF

Answer: p16INK4 (also known as CDKN2A)
Exact answer: p16INK4