Results 31 to 40 of about 100,521 (261)
DOT1L as a central epigenetic regulator of EndoMT and pulmonary fibrosis. Acting as an early epigenetic switch, it translates TGFβ–SMAD signaling into H3K79me2‐mediated chromatin remodeling, selectively activates fibrosis‐related genes, and primes ECs for rapid mesenchymal transition.
Yaofeng Wang +11 more
wiley +1 more source
Molecular mechanisms of the PRL phosphatases [PDF]
The phosphatases of regenerating liver (PRLs) are an intriguing family of dual specificity phosphatases due to their oncogenicity. The three members are small, single domain enzymes. We provide an overview of the phosphatases of regenerating liver, compare them to related phosphatases, and review recent reports about each phosphatase.
Pablo, Rios, Xun, Li, Maja, Köhn
openaire +2 more sources
Neuronal PKM2‐driven glycolysis generates excess lactate that triggers histone H3K18 lactylation (H3K18la), establishing a pathogenic metabolic‐epigenetic axis in epilepsy. Elevated H3K18la enriches the Cop1 promoter, transcriptionally upregulating the E3 ubiquitin ligase COP1, which subsequently drives proteasomal degradation of GABAARβ2 and impairs ...
Yuan Meng +8 more
wiley +1 more source
PRL-3: A metastasis-associated phosphatase in search of a function
The molecular and cellular events involved in cancer progression and metastasis remain much less well-defined than those involved in oncogenesis, despite the fact that cell metastasis is the major factor in cancer mortality.
Bessette, Darrell C. +2 more
core +1 more source
MicroRNAs (MiRNAs) play critical roles in the regulation of pituitary function. MiR-130a-3p has previously been found to be down-regulated in prolactinoma, but its roles in prolactin (PRL) regulation and the underlying mechanisms are still unclear.
Yongliang Zhang (122202) +8 more
core +1 more source
CD4+ Tregs Drive Post‐Ischemic Sprouting Angiogenesis via Endothelial YY1/MAML1 Reactivation
ABSTRACT Microvascular complications of diabetes are chronic diseases of small vessels. We previously found that CD4+ regulatory T‐cells (Tregs) are markedly reduced in type 2 diabetes (T2D) after ischemic injury in both mice and humans, and that Treg deficiency in immunodeficient mice impairs vascular regeneration.
Hang Qu +10 more
wiley +1 more source
Development of Anti-PRL (Prolactin) Autoantibodies by Homologous PRL in Rats: A Model for Macroprolactinemia [PDF]
Macroprolactinemia is hyperprolactinemia in humans mainly due to anti-PRL (prolactin) autoantibodies and is a pitfall for the differential diagnosis of hyperprolactinemia. Despite its high prevalence, the pathogenesis remains unclear. In this study, we examined whether anti-PRL autoantibodies develop via immunization with homologous rat pituitary PRL ...
Naoki, Hattori +4 more
openaire +2 more sources
Model of circNrip1 (cNrip1) upregulation driving neuropathic pain mechanisms. After peripheral nerve injury, increased FUS triggers the formation and upregulation of cNrip1 in injured DRG neurons. Upregulated cNrip1 recruits SYNCRIP to the 3′‐UTR of Tlr2 mRNA by binding to both, thereby promoting SYNCRIP‐triggered Tlr2 mRNA stability and increasing ...
Xiaozhou Feng +14 more
wiley +1 more source
Anti-prolactin (PRL) autoantibody-binding sites (epitopes) on PRL molecule in macroprolactinemia [PDF]
Macroprolactinemia, in which serum prolactin (PRL) mainly consists of PRL with a molecular mass greater than 100 kDa, has been demonstrated to be associated with hyperprolactinemia. We previously reported that anti-PRL autoantibody is the major cause of macroprolactinemia.
N, Hattori +5 more
openaire +2 more sources
Pancreatic neuroendocrine tumors frequently silence MEN1 through epigenetic mechanisms. Here, SIRT7 recruits DNMT1 to the MEN1 promoter, drives hypermethylation, and enhances DNA repair. Inhibiting SIRT7 restores MEN1, reduces MRN complex abundance, impairs double‐strand break repair, and sensitizes PanNET models to radiation, supporting SIRT7 as a ...
Jianyun Jiang +11 more
wiley +1 more source

