Aberrant gene expression in cultured mammalian bone cells demonstrates an osteoblast defect in osteopetrosis

1994 ◽  
Vol 55 (3) ◽  
pp. 366-372 ◽  
Author(s):  
M. E. Jackson ◽  
V. Shalhoub ◽  
J. B. Lian ◽  
G. S. Stein ◽  
S. C. Marks
Keyword(s):  
Gene Expression ◽  
Bone Cells ◽  
Aberrant Gene Expression ◽  
Aberrant Gene ◽  
Mammalian Bone

scholarly journals Publisher Correction to: C11orf95-RELA fusion drives aberrant gene expression through the unique epigenetic regulation for ependymoma formation

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Tatsuya Ozawa ◽  
Syuzo Kaneko ◽  
Frank Szulzewsky ◽  
Zhiwei Qiao ◽  
Mutsumi Takadera ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epigenetic Regulation ◽  
Aberrant Gene Expression ◽  
Aberrant Gene

An amendment to this paper has been published and can be accessed via the original article.

scholarly journals Transcriptome analysis identified aberrant gene expression in pollen developmental pathways leading to CGMS in cotton (Gossypium hirsutum L.)

PLoS ONE ◽  
2019 ◽  
Vol 14 (6) ◽  
pp. e0218381 ◽  
Author(s):  
Rasmieh Hamid ◽  
Hassan Marashi ◽  
Rukam S. Tomar ◽  
Saeid Malekzadeh Shafaroudi ◽  
Pritesh H. Sabara
Keyword(s):  
Gene Expression ◽  
Gossypium Hirsutum ◽  
Transcriptome Analysis ◽  
Developmental Pathways ◽  
Gossypium Hirsutum L ◽  
Aberrant Gene Expression ◽  
Aberrant Gene

scholarly journals Lineage promiscuity in hemopoietic differentiation and leukemia

Blood ◽  
1986 ◽  
Vol 67 (1) ◽  
pp. 1-11 ◽  
Author(s):  
MF Greaves ◽  
LC Chan ◽  
AJ Furley ◽  
SM Watt ◽  
HV Molgaard
Keyword(s):  
Gene Expression ◽  
Cell Receptor ◽  
Leukemic Cells ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Aberrant Gene Expression ◽  
Lineage Infidelity ◽  
T Cell Receptor Genes ◽  
Bona Fide ◽  
Aberrant Gene ◽  
Ig Heavy Chain

An increasing number of reports document instances in which individual leukemic cells coexpress markers normally believed to be restricted to a single lineage. This has been interpreted by McCulloch and colleagues as aberrant programming or lineage infidelity and contrasts with earlier suggestions that lineage fidelity of gene expression was usually maintained in leukemia. We argue that several examples of infidelity are suspect on technical grounds, whereas others are bona fide and require explanation, eg, partial rearrangements and expression of Ig heavy-chain and/or T cell receptor genes in inappropriate cells and terminal deoxynucleotidyl transferase in leukemic myeloblasts. Individual examples of truly aberrant gene expression may well occur in leukemia but with insufficient regularity to be of general significance. We suggest that verifiable and consistent examples of apparent lineage infidelity do not reflect genetic misprogramming but rather the existence of a transient phase of limited promiscuity of gene expression occurring in normal biopotential or multipotential progenitors and able to be preserved as a relic in leukemic blast cell populations that are in maturation arrest. This alternative explanation has interesting implications for mechanisms of hematopoietic differentiation and leads to some testable predictions.

scholarly journals Spatiotemporal gating of SIRT1 functions by O-GlcNAcylation is essential for liver metabolic switching and prevents hyperglycemia

2020 ◽  
Vol 117 (12) ◽  
pp. 6890-6900 ◽  
Author(s):  
Tandrika Chattopadhyay ◽  
Babukrishna Maniyadath ◽  
Hema P. Bagul ◽  
Arindam Chakraborty ◽  
Namrata Shukla ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Nutrient Inputs ◽  
Fed State ◽  
Physiological Fitness ◽  
Metabolic Switching ◽  
Nuclear Exclusion ◽  
Aberrant Gene Expression ◽  
Systemic Insulin Resistance ◽  
Aberrant Gene

Inefficient physiological transitions are known to cause metabolic disorders. Therefore, investigating mechanisms that constitute molecular switches in a central metabolic organ like the liver becomes crucial. Specifically, upstream mechanisms that control temporal engagement of transcription factors, which are essential to mediate physiological fed–fast–refed transitions are less understood. SIRT1, a NAD+-dependent deacetylase, is pivotal in regulating hepatic gene expression and has emerged as a key therapeutic target. Despite this, if/how nutrient inputs regulate SIRT1 interactions, stability, and therefore downstream functions are still unknown. Here, we establish nutrient-dependent O-GlcNAcylation of SIRT1, within its N-terminal domain, as a crucial determinant of hepatic functions. Our findings demonstrate that during a fasted-to-refed transition, glycosylation of SIRT1 modulates its interactions with various transcription factors and a nodal cytosolic kinase involved in insulin signaling. Moreover, sustained glycosylation in the fed state causes nuclear exclusion and cytosolic ubiquitin-mediated degradation of SIRT1. This mechanism exerts spatiotemporal control over SIRT1 functions by constituting a previously unknown molecular relay. Of note, loss of SIRT1 glycosylation discomposed these interactions resulting in aberrant gene expression, mitochondrial dysfunctions, and enhanced hepatic gluconeogenesis. Expression of nonglycosylatable SIRT1 in the liver abrogated metabolic flexibility, resulting in systemic insulin resistance, hyperglycemia, and hepatic inflammation, highlighting the physiological costs associated with its overactivation. Conversely, our study also reveals that hyperglycosylation of SIRT1 is associated with aging and high-fat–induced obesity. Thus, we establish that nutrient-dependent glycosylation of SIRT1 is essential to gate its functions and maintain physiological fitness.

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