Dhaliwal et al., KLF4 protein stability regulated by interaction with pluripotency
transcription factors overrides transcriptional control.
Citation: Peng Liu et al., "CRISPR-Based Chromatin Remodeling of the Endogenous Oct4 or Sox2 Locus Enables Reprogramming to Pluripotency
," Cell Stem Cell, 2018; DOI: 10.1016/j.stem.2017.12.001
This unique developmental licensing of pluripotency
is likely partially responsible for the extremely heterogeneous histological variation amongst germ cell tumors.
Moreover, cESCs with pluripotency
potential were still observed after 48 passages (over 260 days; figure not shown).
OCT4 is a crucial and dependent determinant of pluripotency
in ES and EC cells (10).
It has also been reported that inhibition of oxidative pathways is important to maintain pluripotency
, and we demonstrated that hypoxia directly promotes cell reprogramming of in vivo committed cells .
The researchers looked at the molecular signals that control TET activity to understand more about how the activity of the TET enzymes can be manipulated during cellular programming to achieve pluripotency
The capacity for self-renewal and the pluripotency
of ESCs is known to be controlled by the transcription factors, Nanog homeobox (NANOG), octamer binding transcription factor-4 (OCT4) and sex determining region-Y box-2 (SOX2), and signaling pathways like leukemia inhibitory factor (LIF)-signal transducer and activator of transcription 3 (STAT3) and bone morphogenic protein (BMP)-Mothers against decapentaplegic homolog (SMAD) 1/4/5/8 (Rodda et al., 2005).
Cancer, biology, and genetics researchers from North America and Europe discuss the MYC protein and its regulation of expression, protein-protein interactions, genomic recognition, and transcriptional functions; MYC's biological activities in normal cellular processes, including its roles in pluripotency
, vertebrate and invertebrate development, DNA replication, apoptosis, and metabolism; the activities that make it a major driver in oncogenicity, including its regulatory mutations, induction of genomic instability, cell competition, and metabolic programming; specific examples of its roles in Burkitt lymphoma, medulloblastoma, and neuroblastoma; and approaches to tumors, including synthetic lethal screens and targeted chemotherapy.
After a five-month investigation by the Riken Center for Developmental Biology of two stress-triggered acquisition of pluripotency
(STAP) cell studies in the journal Nature, the papers were retracted in early July.
The retraction states: "These multiple errors impair the credibility of the study as a whole and we are unable to say without doubt whether the stimulus-triggered acquisition of pluripotency
stem cells phenomenon is real.