GoPubMed Proteins lists recent and important papers and reviews for
proteins. Page last changed on 19 Dec 2016.
Elongation factor RNA polymerase II
MEN, ELL
Malate dehydrogenase catalyzes the reversible oxidation of malate to oxaloacetate, utilizing the NAD/NADH cofactor system in the citric acid cycle. The protein encoded by this gene is localized to the mitochondria and may play pivotal roles in the malate-aspartate shuttle that operates in the metabolic coordination between cytosol and mitochondria. [provided by RefSeq, Jul 2008] (from
NCBI)
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Top mentioned proteins:
RET, CAN, Multiple Endocrine Neoplasia, HAD, AGE
Papers on
MEN
Animal models of multiple endocrine neoplasia.
Review
New
München, Germany. In Mol Cell Endocrinol, Mar 2016
Multiple endocrine neoplasia (MEN) syndromes are autosomal dominant diseases with high penetrance characterized by proliferative lesions (usually hyperplasia or adenoma) arising in at least two endocrine tissues.
A 6 bp In Frame Germline Deletion In Exon 7 Of RET Leads To Increased RET Phosphorylation, ERK Activation And MEN2A.
New
Essen, Germany. In J Clin Endocrinol Metab, Feb 2016
CONTEXT: Multiple endocrine neoplasia (MEN) 2 is usually caused by missense mutations in the proto-oncogene RET.
Distribution of RET Mutations and Evaluation of Treatment Approaches in Hereditary Medullary Thyroid Carcinoma in Turkey.
New
In J Clin Res Pediatr Endocrinol, Jan 2016
An evaluation form was sent to physicians of eligible 319 patients who had confirmed sporadic MTC, familial MTC, MEN 2 or mutation carriers.
Uncommon association of cerebral meningioma, parathyroid adenoma and papillary thyroid carcinoma in a patient harbouring a rare germline variant in the CDKN1B gene.
New
Lisbon, Portugal. In Bmj Case Rep, Dec 2015
Multiple endocrine neoplasia type 4 (MEN 4) is a novel form of multiple endocrine neoplasia caused by mutations in the CDKN1B gene.
Multiple Endocrine Neoplasia: Genetics and Clinical Management.
Review
New
Stanford, United States. In Surg Oncol Clin N Am, Oct 2015
Early diagnosis of multiple endocrine neoplasia (MEN) syndromes is critical for optimal clinical outcomes; before the MEN syndromes can be diagnosed, they must be suspected.
Clinicopathological correlates of hyperparathyroidism.
Review
New
Toronto, Canada. In J Clin Pathol, Oct 2015
While most cases (95%) occur sporadically, about 5% are associated with a hereditary syndrome: multiple endocrine neoplasia syndromes (MEN-1, MEN-2A, MEN-4), hyperparathyroidism-jaw tumour syndrome (HPT-JT), familial hypocalciuric hypercalcaemia (FHH-1, FHH-2, FHH-3), familial hypercalciuric hypercalcaemia, neonatal severe hyperparathyroidism and isolated familial hyperparathyroidism.
Pheochromocytomas and Paragangliomas: An Update on Recent Molecular Genetic Advances and Criteria for Malignancy.
Review
New
Hangzhou, China. In Adv Anat Pathol, Sep 2015
Molecular genetic studies in the past few years have identified >10 genes involved in the pathogenesis of pheochromocytomas and paragangliomas, including RET oncogene, involved in the pathogenesis of multiple endocrine neoplasia (MEN) 2A and 2B, von Hippel-Lindau tumor-suppressor gene, neurofibromatosis type 1 gene, succinate dehydrogenase, THEM127, and several others.
[APPLICATION OF INTEGRAL INDICATOR FOR ASSESSMENT OF OXIDATIVE STRESS IN MEN WITH PATHOSPERMIA AND TYPE 1 DIABETES].
New
In Urologiia, Jul 2015
This study introduces a method for assessing the individual degree of oxidative stress (integral indicator) in men with pathospermia and type 1 diabetes, based on lipid peroxidation parameters.
[SMOKING AS A TRIGGER FACTOR IN THE DEVELOPMENT OF DIABETIC ANGIOPATHY OF LOWER EXTREMITIES IN MEN WITH METHYLENETETRAHYDROFOLATEREDUCTASE 677TT GENOTYPE].
In Klin Med (mosk), 2014
The aim of this work was to elucidate the relationship between the functionally significant methylenetetrahydroxyfolatereductase (MTHFR) C677T (rs1801133) gene polymorphism and the development of diabetic angiopathy of lower extremities (DALE) in ethnic Russian men residing in Central Russia (mostly Kursk region).
Mechanosensitivity in the enteric nervous system.
Review
Freising, Germany. In Front Cell Neurosci, 2014
Mechanosensitive enteric neurons (MEN) initiate reflex activity by responding to mechanical deformation of the gastrointestinal wall.
Cancer-associated osteoclast differentiation takes a good look in the miR(NA)ror.
Impact
Indianapolis, United States. In Cancer Cell, 2013
In this issue of Cancer Cell, Ell and colleagues show how a discrete miRNA network regulates osteoclastogenesis during breast cancer bone metastasis.
Activation of the yeast Hippo pathway by phosphorylation-dependent assembly of signaling complexes.
Impact
Cambridge, United States. In Science, 2013
In budding yeast, one such signal transduction pathway called the mitotic exit network (MEN) governs the transition from mitosis to the G1 phase of the cell cycle.
The RNA Pol II elongation factor Ell3 marks enhancers in ES cells and primes future gene activation.
Impact
Kansas City, United States. In Cell, 2013
We have found that Ell3, a member of the Ell (eleven-nineteen lysine-rich leukemia gene) family of RNA Pol II elongation factors, occupies enhancers in embryonic stem cells.
The super elongation complex (SEC) family in transcriptional control.
Review
Impact
GeneRIF
Kansas City, United States. In Nat Rev Mol Cell Biol, 2012
Studies indicate that the super elongation complex (SEC) consisting of ELL, P-TEFb (CDK9) and MLL required for rapid transcriptional induction in the presence or absence of paused RNA polymerase II (Pol II).
The S. pombe cytokinesis NDR kinase Sid2 activates Fin1 NIMA kinase to control mitotic commitment through Pom1/Wee1.
Impact
Manchester, United Kingdom. In Nat Cell Biol, 2012
The mitotic exit network (MEN) of budding yeast regulates both processes, whereas the fission yeast equivalent, the septum initiation network (SIN), controls only the execution of cytokinesis.
ELL facilitates RNA polymerase II pause site entry and release.
GeneRIF
Bethesda, United States. In Nat Commun, 2011
ELL has an early and essential role during rapid high-amplitude gene expression that is required for both Pol II pause site entry and release
ELL is an HIF-1alpha partner that regulates and responds to hypoxia response in PC3 cells.
GeneRIF
Beijing, China. In Prostate, 2010
Our findings suggest that ELL and HIF-1alpha are binding partners and can modulate the functions of each other in hypoxia.
Elongation factor ELL (Eleven-Nineteen Lysine-rich Leukemia) acts as a transcription factor for direct thrombospondin-1 regulation.
GeneRIF
Wuhan, China. In J Biol Chem, 2009
ELL (Eleven-Nineteen Lysine-rich Leukemia) acts as a transcription factor for direct thrombospondin-1 regulation
Regulation of the transcriptional activity of poised RNA polymerase II by the elongation factor ELL.
GeneRIF
Kansas City, United States. In Proc Natl Acad Sci U S A, 2008
elongation factor ELL protein regulates the transcription activvity of RNA polymerase II
