A human homolog of mouse Lbh gene, hLBH, expresses in heart and activates SRE and AP-1 mediated MAPK signaling pathway

Ai, Jianping; Wang, Yuequn; Tan, Kai; Deng, Yuan; Luo, Na; Yuan, Wuzhou; Wang, Zequn; Li, Yongqing; Wang, Ying; Mo, Xiaoyang; Zhu, Chuanbing; Yin, Zhaochu; Liu, Mingyao; Wu, Xiushan

doi:10.1007/s11033-007-9068-4

Cited by 34 publications

(37 citation statements)

References 21 publications

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“…4A). It is known that p21 is one of the downstream genes of p53 and p53 strongly induces p21 expression (13). As expected, the stronger repression effect on the activity of p53 is obseved when overexpression of CRYAB and LBH together compared to transfection of LBH or CRYAB alone.…”

Section: Discussionsupporting

confidence: 71%

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Synergistic efficacy of LBH and αB-crystallin through inhibiting transcriptional activities of p53 and p21

Deng¹,

Li²,

Fan³

et al. 2010

BMB Reports

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LBH is a transcription factor as a candidate gene for CHD associated with partial trisomy 2p syndrome. To identify potential LBH-interacting partners, a yeast two-hybrid screen using LBH as a bait was performed with a human heart cDNA library. One of the clones identified encodes αB-crystallin. Co-immunoprecipitation and GST pull-down assays showed that LBH interacts with αB-crystallin, which is further confirmed by mammalian two-hybrid assays. Co-localization analysis showed that in COS-7 cells, αB-crystallin that is cytoplasmic alone, accumulates partialy in the nucleus when co-transfected with LBH. Transient transfection assays indicated that overexpression of LBH or αB-crystallin reduced the transcriptional activities of p53 and p21, respectively, Overexpression of both αB-crystallin and LBH together resulted in a stronger repression of the transcriptional activities of p21 and p53. These results showed that the interaction of LBH and αB-crystallin may inhibit synergistically the transcriptional regulation of p53 and p21. [BMB reports 2010; 43(6): 432-437]

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Section: Discussionsupporting

confidence: 71%

“…Recently, we have cloned and characterized the human LBH gene that is most abundantly expressed in embryonic and adult heart (13). To identify potential LBH-interacting partners, a yeast two-hybrid screen using LBH as a bait was performed with a human heart cDNA library.…”

Section: Introductionmentioning

confidence: 99%

Synergistic efficacy of LBH and αB-crystallin through inhibiting transcriptional activities of p53 and p21

Deng¹,

Li²,

Fan³

et al. 2010

BMB Reports

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“…The FOS transcription factor family has pleiotropic cellular effects. LBH recruits Pol II to specific promoter sites and may regulate FOS through the serum-responsive element (SRE) in the FOS promoter (27). OSR2 regulates genes involved in proliferation and development (28).…”

Section: Abu-specific Changes In Gene Expressionmentioning

confidence: 99%

Bacterial control of host gene expression through RNA polymerase II

Lutay¹,

Ambite²,

Hernández³

et al. 2013

J. Clin. Invest.

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The normal flora furnishes the host with ecological barriers that prevent pathogen attack while maintaining tissue homeostasis. Urinary tract infections (UTIs) constitute a highly relevant model of microbial adaptation in which some patients infected with Escherichia coli develop acute pyelonephritis, while other patients with bacteriuria exhibit an asymptomatic carrier state similar to bacterial commensalism. It remains unclear if the lack of destructive inflammation merely reflects low virulence or if carrier strains actively inhibit disease-associated responses in the host. Here, we identify a new mechanism of bacterial adaptation through broad suppression of RNA polymerase II-dependent (Pol II-dependent) host gene expression. Over 60% of all genes were suppressed 24 hours after human inoculation with the prototype asymptomatic bacteriuria (ABU) strain E. coli 83972, and inhibition was verified by infection of human cells. Specific repressors and activators of Pol II-dependent transcription were modified, Pol II phosphorylation was inhibited, and pathogen-specific signaling was suppressed in cell lines and inoculated patients. An increased frequency of strains inhibiting Pol II was epidemiologically verified in ABU and fecal strains compared with acute pyelonephritis, and a Pol II antagonist suppressed the disease-associated host response. These results suggest that by manipulating host gene expression, ABU strains promote tissue integrity while inhibiting pathology. Such bacterial modulation of host gene expression may be essential to sustain asymptomatic bacterial carriage by ensuring that potentially destructive immune activation will not occur.

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“…LBH was identified originally as a transcriptional coactivator involved in the molecular signaling pathways of heart and limb development [9, 22]. Other studies have confirmed that LBH plays an important role in embryonic development [23, 24]. Over the years, researchers have found it to be associated with several autoimmune diseases, including systemic lupus erythematosus and rheumatoid arthritis [25-30].…”

Section: Discussionmentioning

confidence: 99%

Limb-Bud and Heart Attenuates Growth and Invasion of Human Lung Adenocarcinoma Cells and Predicts Survival Outcome

Deng

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: The transcription cofactor limb-bud and heart (LBH) is involved in embryonic development. However, its role in human lung cancer, especially lung adenocarcinoma (LUAD), remains unclear. Methods: A public database and tissue microarray (TMA) were used to compare differences in LBH expression and its relationship with clinical characteristics. Tissue from an additional 70 LUAD patients with follow-up records was used to explore the correlation of LBH expression with prognosis. Cellular and molecular studies validated the role of LBH in LUAD growth and invasion. Results: LBH was significantly down-regulated in lung cancer tissue samples and was correlated with the prognosis and clinical characteristics of lung cancer patients based on a public database and TMA. Survival analysis revealed that LBH-negative expression was associated with poor overall survival of LUAD patients (P = 0.021). Cox regression analysis showed that LBH expression status was a favorable independent prognostic factor (hazard ratio = 0.120, 95% confidence interval = 0.016–0.894, P = 0.039). LBH knockdown accelerated LUAD cell proliferation, migration, and invasion. Furthermore, bioinformatics analysis indicated that LBH was significantly related to the cell adhesion pathway. Western blot analysis confirmed that LBH could regulate the expression of integrin family members (integrin-α1, integrin-α2, integrin-α4, integrin-αv, and integrin-β4). Conclusion: Our data suggest that LBH plays an important role in lung cancer. Importantly, LBH is an independent prognostic factor in LUAD and can attenuate cell growth and invasion. LBH may be a potential prognostic biomarker in LUAD patients.

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A human homolog of mouse Lbh gene, hLBH, expresses in heart and activates SRE and AP-1 mediated MAPK signaling pathway

Cited by 34 publications

References 21 publications

Synergistic efficacy of LBH and αB-crystallin through inhibiting transcriptional activities of p53 and p21

Synergistic efficacy of LBH and αB-crystallin through inhibiting transcriptional activities of p53 and p21

Bacterial control of host gene expression through RNA polymerase II

Limb-Bud and Heart Attenuates Growth and Invasion of Human Lung Adenocarcinoma Cells and Predicts Survival Outcome

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