C/EBPγ Suppresses Senescence and Inflammatory Gene Expression by Heterodimerizing with C/EBPβ

Huggins, Christopher J.; Malı́k, Radek; Lee, Sook; Salotti, Jacqueline; Thomas, Sara; Martín, Nancy; Quiñones, Octavio A.; Alvord, W. Gregory; Olanich, Mary E.; Keller, Jonathan R.; Johnson, Peter F.

doi:10.1128/mcb.01674-12

Cited by 81 publications

(85 citation statements)

References 47 publications

(83 reference statements)

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“…In addition to the CEBPB association with muscle discussed above, CEBPD has also been linked to differential expression of myostatin, a skeletal muscle inhibitory factor that can lead to muscle strength declines (Allen et al ., 2010). CEBPG likely plays a role in cell growth arrest in the setting of inflammation activation (Huggins et al ., 2013). NF‐kB is the nuclear transcription factor that acts as a gate‐keeping molecule for activation of inflammatory signaling (Guttridge et al ., 2000; Ershler, 2007).…”

Section: Discussionmentioning

confidence: 99%

GWAS analysis of handgrip and lower body strength in older adults in the CHARGE consortium

et al. 2016

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SummaryDecline in muscle strength with aging is an important predictor of health trajectory in the elderly. Several factors, including genetics, are proposed contributors to variability in muscle strength. To identify genetic contributors to muscle strength, a meta‐analysis of genomewide association studies of handgrip was conducted. Grip strength was measured using a handheld dynamometer in 27 581 individuals of European descent over 65 years of age from 14 cohort studies. Genomewide association analysis was conducted on ~2.7 million imputed and genotyped variants (SNPs). Replication of the most significant findings was conducted using data from 6393 individuals from three cohorts. GWAS of lower body strength was also characterized in a subset of cohorts. Two genomewide significant (P‐value< 5 × 10−8) and 39 suggestive (P‐value< 5 × 10−5) associations were observed from meta‐analysis of the discovery cohorts. After meta‐analysis with replication cohorts, genomewide significant association was observed for rs752045 on chromosome 8 (β = 0.47, SE = 0.08, P‐value = 5.20 × 10−10). This SNP is mapped to an intergenic region and is located within an accessible chromatin region (DNase hypersensitivity site) in skeletal muscle myotubes differentiated from the human skeletal muscle myoblasts cell line. This locus alters a binding motif of the CCAAT/enhancer‐binding protein‐β (CEBPB) that is implicated in muscle repair mechanisms. GWAS of lower body strength did not yield significant results. A common genetic variant in a chromosomal region that regulates myotube differentiation and muscle repair may contribute to variability in grip strength in the elderly. Further studies are needed to uncover the mechanisms that link this genetic variant with muscle strength.

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Section: Discussionmentioning

confidence: 99%

GWAS analysis of handgrip and lower body strength in older adults in the CHARGE consortium

et al. 2016

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“…The knockdown vector for Cebpb (Cebpb1 shRNA) has been described previously (5). Dominant negative Egr1 is a truncated form containing the zinc finger domain (residues 329 to 425) as described by Chapman and Perkins (17).…”

Section: Methodsmentioning

confidence: 99%

“…In addition to exhibiting growth arrest and positive staining for SA-␤Gal, senescent cells express and secrete senescence-associated secretory phenotype (SASP) factors, some of which are direct targets of C/EBP␤ (4,5,11,23). In 3T3…”

Section: Ectopic Expression Of Egr Proteins Induces Growth Arrest Andmentioning

confidence: 99%

“…In response to Ras-Raf-MEK-extracellular signal-regulated kinase (ERK) signaling, C/EBP␤ becomes posttranslationally activated and displays increased DNA binding and homodimerization (5,6). In this activated state, C/EBP␤ inhibits cell proliferation and induces expression of senescence-associated secretory phenotype (SASP) genes, which encode inflammatory cytokines, chemokines, and their receptors (4,5,7,8). C/EBP␤ is required for OIS in some contexts as genetic or RNA interference (RNAi)-mediated ablation of C/EBP␤ allows primary fibroblasts to bypass oncogene-induced arrest.…”

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confidence: 99%

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An Arf-Egr-C/EBPβ Pathway Linked to Ras-Induced Senescence and Cancer

Salotti

Sakchaisri

Tourtellotte

et al. 2015

Molecular and Cellular Biology

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“…We therefore concluded that the 33 kDa band represented LAP and the 37 kDa band LAP*, as previous studies indicated that p33 is mainly translated in mouse embryonic fibroblasts (MEF), NIH3T3, and 3T3-L1 cells. (30)(31)(32)(33) No band corresponding to LIP was detected (data not shown). Mouse C/EBPb is known to be localized in the nucleus, which was confirmed by immunostaining using 7H5 and 7D2 monoclonal antibody clones (Fig.…”

Section: Resultsmentioning

confidence: 99%

Production of a Monoclonal Antibody for C/EBPβ: The Subnuclear Localization of C/EBPβ in Mouse L929 Cells

Harada

Okazaki

Okada

et al. 2014

Monoclonal Antibodies in Immunodiagnosis and Immunotherapy

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C/EBPγ Suppresses Senescence and Inflammatory Gene Expression by Heterodimerizing with C/EBPβ

Cited by 81 publications

References 47 publications

GWAS analysis of handgrip and lower body strength in older adults in the CHARGE consortium

GWAS analysis of handgrip and lower body strength in older adults in the CHARGE consortium

An Arf-Egr-C/EBPβ Pathway Linked to Ras-Induced Senescence and Cancer

Production of a Monoclonal Antibody for C/EBPβ: The Subnuclear Localization of C/EBPβ in Mouse L929 Cells

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