Publications

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Name: Haifeng Yang, PhD
Position: Assistant Professor

1020 Locust Street
336D JAH
Philadelphia, PA 19107

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Highlighted Publications

Xiaohua Niu, Ting Zhang, Lili Liao, Liang Zhou, Ming Zhou, Daniel J. Lindner, Brian Rini, Qin Yan, Haifeng Yang. 2011. The von Hippel-Lindau Tumor Suppressor Protein Regulates Gene Expression and Tumorigenesis through Histone Demethylase JARID1C.  2012. Oncogene. 31(6):776-86.

This paper explained that activated HIF, as a result of VHL loss, caused the activation of a histone demethylase, JARID1C. In turn JARID1C changed transcription and repressed tumor growth, constituting a negative feedback loop. This provided the pressure to mutate JARID1C in kidney cancer.

Liang Zhou, Haifeng Yang. 2011. The von Hippel-Lindau Tumor Suppressor Protein Promotes c-Cbl-independent poly-ubiquitylation and degradation of the activated EGFR. 2011. PLoS One. 6(9):e23936. 

This article discovered that pVHL could target the activated EGFR for degration. This suggested that in VHL-defective cells EGFR is more activated and contributed to enhanced tumor growth.

Ting Zhang, Xiaohua Niu, Lili Liao, Eun-Ah Cho, Haifeng Yang. 2013. The Contributions of HIF-target Genes to Tumor Growth in RCC.      PLoS One.  8(11):e80544.

This paper revealed that some HIF-target genes are not tumor-promoting. Instead they had anti-tumor effects. This suggested that enhancing the expression of some HIF-target genes could be a way to treat kidney cancer.

Recent Publications

Data supporting the roles of BAP1, STING, and IFN-β in ISGF3 activation in ccRCC

The convergence of tumor suppressors on the type I interferon pathway in clear cell renal cell carcinoma and its therapeutic implications

BAP1 maintains HIF-dependent interferon beta induction to suppress tumor growth in clear cell renal cell carcinoma

Erratum: Correction: Multiple tumor suppressors regulate a HIF-dependent negative feedback loop via ISGF3 in human clear cell renal cancer (eLife (2018) 7 PII: e69256)

PBRM1 suppresses tumor growth as a novel p53 acetylation reader

PBRM1 acts as a p53 lysine-acetylation reader to suppress renal tumor growth

Oxygen sensing and adaptability won the 2019 Nobel Prize in Physiology or medicine

High affinity binding of H3K14ac through collaboration of bromodomains 2, 4 and 5 is critical for the molecular and tumor suppressor functions of PBRM1

Multiple tumor suppressors regulate a hif-dependent negative feedback loop via ISGF3 in human clear cell renal cancer

Intratumoral heterogeneity analysis reveals hidden associations between protein expression losses and patient survival in clear cell renal cell carcinoma

Immunohistochemistry successfully uncovers intratumoral heterogeneity and widespread co-losses of chromatin regulators in clear cell renal cell carcinoma

The structure and regulation of Cullin 2 based E3 ubiquitin ligases and their biological functions

The roles of chromatin-remodelers and epigenetic modifiers in kidney cancer

The contributions of HIF-target genes to tumor growth in RCC

The roles of VHL-dependent ubiquitination in signaling and cancer

The von Hippel-Lindau tumor suppressor protein regulates gene expression and tumor growth through histone demethylase JARID1C

The von hippel-lindau tumor suppressor protein promotes c-Cbl-independent poly-ubiquitylation and degradation of the activated EGFR

pVHL Acts as an Adaptor to Promote the Inhibitory Phosphorylation of the NF-κB Agonist Card9 by CK2

Neuronal apoptosis linked to EglN3 prolyl hydroxylase and familial pheochromocytoma genes: Developmental culling and cancer

Analysis of von Hippel-Lindau Hereditary Cancer Syndrome: Implications of Oxygen Sensing

Biochemical purification and pharmacological inhibition of a mammalian prolyl hydroxylase acting on hypoxia-inducible factor

Structure of an HIF-1α-pVHL complex: Hydroxyproline recognition in signaling

Molecular pathogenesis of the von Hippel-Lindau hereditary cancer syndrome: Implications for oxygen sensing

Von Hippel-Lindau protein mutants linked to type 2C VHL disease preserve the ability to downregulate HIF

HIFα targeted for VHL-mediated destruction by proline hydroxylation: Implications for O2 sensing

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