Log in

Relevant bibliographies by topics / Hedgehog interacting protein / Journal articles

Journal articles on the topic 'Hedgehog interacting protein'

To see the other types of publications on this topic, follow the link: Hedgehog interacting protein.

Author: Grafiati

Published: 10 December 2022

Last updated: 29 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Hedgehog interacting protein.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Vogt, Annika, Pao-Tien Chuang, Jennifer Hebert, Jimmy Hwang, Ying Lu, Levy Kopelovich, Mohammad Athar, David R. Bickers, and Ervin H. Epstein. "Immunoprevention of Basal Cell Carcinomas with Recombinant Hedgehog-interacting Protein." Journal of Experimental Medicine 199, no. 6 (March 15, 2004): 753–61. http://dx.doi.org/10.1084/jem.20031190.

Full text

Abstract:

Basal cell carcinomas (BCCs) are driven by abnormal hedgehog signaling and highly overexpress several hedgehog target genes. We report here our use of one of these target genes, hedgehog-interacting protein (Hip1), as a tumor-associated antigen for immunoprevention of BCCs in Ptch1+/− mice treated with ionizing radiation. Hip1 mRNA is expressed in adult mouse tissues at levels considerably lower than those in BCCs. Immunization with either of two large recombinant Hip1 polypeptides was well tolerated in Ptch1+/− mice, induced B and T cell responses detectable by enzyme-linked immunosorbent assay, Western blot, delayed type hypersensitivity, and enzyme-linked immunospot assay, and reduced the number of BCCs by 42% (P < 0.001) and 32% (P < 0.01), respectively. We conclude that immunization with proteins specifically up-regulated by hedgehog signaling may hold promise as a preventive option for patients such as those with the basal cell nevus syndrome who are destined to develop large numbers of BCCs.

APA, Harvard, Vancouver, ISO, and other styles

2

Bishop, Benjamin, A. Radu Aricescu, Karl Harlos, Chris A. O'Callaghan, E. Yvonne Jones, and Christian Siebold. "Structural insights into hedgehog ligand sequestration by the human hedgehog-interacting protein HHIP." Nature Structural & Molecular Biology 16, no. 7 (June 28, 2009): 698–703. http://dx.doi.org/10.1038/nsmb.1607.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Sekiguchi, Haruki, Masaaki Ii, Kentaro Jujo, Marie-Ange Renault, Tina Thorne, Trevor Clarke, Aiko Ito, et al. "Estradiol triggers sonic-hedgehog-induced angiogenesis during peripheral nerve regeneration by downregulating hedgehog-interacting protein." Laboratory Investigation 92, no. 4 (February 13, 2012): 532–42. http://dx.doi.org/10.1038/labinvest.2012.6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Tojo, M., H. Kiyosawa, K. Iwatsuki, and F. Kaneko. "Expression of a sonic hedgehog signal transducer, hedgehog-interacting protein, by human basal cell carcinoma." British Journal of Dermatology 146, no. 1 (January 2002): 69–73. http://dx.doi.org/10.1046/j.1365-2133.2002.04583.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Cobourne, Martyn, and Paul Sharpe. "Expression and Regulation of Hedgehog-Interacting Protein During Early Tooth Development." Connective Tissue Research 43, no. 2 (April 1, 2002): 143–47. http://dx.doi.org/10.1080/713713516.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Cobourne, Martyn T., and Paul T. Sharpe. "Expression and Regulation of Hedgehog-Interacting Protein During Early Tooth Development." Connective Tissue Research 43, no. 2-3 (January 2002): 143–47. http://dx.doi.org/10.1080/03008200290000907.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Van Durme, Y. M. T. A., M. Eijgelsheim, G. F. Joos, A. Hofman, A. G. Uitterlinden, G. G. Brusselle, and B. H. C. Stricker. "Hedgehog-interacting protein is a COPD susceptibility gene: the Rotterdam Study." European Respiratory Journal 36, no. 1 (December 8, 2009): 89–95. http://dx.doi.org/10.1183/09031936.00129509.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Lu, Jiuyi, Minyong Chen, Xiu-Rong Ren, Jiangbo Wang, H. Kim Lyerly, Larry Barak, and Wei Chen. "Regulation of Hedgehog Signaling by Myc-Interacting Zinc Finger Protein 1, Miz1." PLoS ONE 8, no. 5 (May 3, 2013): e63353. http://dx.doi.org/10.1371/journal.pone.0063353.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Coulombe, J., E. Traiffort, K. Loulier, H. Faure, and M. Ruat. "Hedgehog interacting protein in the mature brain: membrane-associated and soluble forms." Molecular and Cellular Neuroscience 25, no. 2 (February 2004): 323–33. http://dx.doi.org/10.1016/j.mcn.2003.10.024.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Kobune, M., S. Iyama, S. Kikuchi, H. Horiguchi, T. Sato, K. Murase, Y. Kawano, et al. "Stromal cells expressing hedgehog-interacting protein regulate the proliferation of myeloid neoplasms." Blood Cancer Journal 2, no. 9 (September 2012): e87-e87. http://dx.doi.org/10.1038/bcj.2012.36.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Li, Xingnan, Timothy D. Howard, Wendy C. Moore, Elizabeth J. Ampleford, Huashi Li, William W. Busse, William J. Calhoun, et al. "Importance of hedgehog interacting protein and other lung function genes in asthma." Journal of Allergy and Clinical Immunology 127, no. 6 (June 2011): 1457–65. http://dx.doi.org/10.1016/j.jaci.2011.01.056.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Kobune, Masayoshi, Hiroto Horiguchi, Shohei Kikuchi, Satoshi Iyama, Kohichi Takada, Kazuyuki Murase, Kaoru Ono, et al. "Stromal Cells Expressing Hedgehog-Interacting Protein Are One of the Main Regulators of the Hedgehog Signaling System in Myeloid Neoplasms." Blood 120, no. 21 (November 16, 2012): 3840. http://dx.doi.org/10.1182/blood.v120.21.3840.3840.

Full text

Abstract:

Abstract Abstract 3840 Aberrant reactivation of Hedgehog (Hh) signaling has been described in a wide variety of human cancers including cancer stem cells. However, involvement of the Hh signaling system in the bone marrow (BM) microenvironment during the development of myeloid neoplasm is unclear. In this study we assessed the expression of Hh-related proteins in normal human CD34+ cells, CD34+ leukemic/dysplastic cells and BM stromal cells. Both Indian hedgehog (Ihh) and its signal transducer, SMO, were expressed in CD34+ acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) derived cells, suggesting that Ihh could be affected in an autocrine manner. Remarkably, expression of the endogenous Hh signaling inhibitor, human hedgehog-interacting protein (HHIP), in AML/MDS-associated stromal cells was significantly lower than in healthy donor-derived stromal cells. Moreover, HHIP expression level in BM stromal cells highly correlated with their tumor-supporting activity of SMO+ leukemic cells. Demethylating agent 5-aza-dC rescued HHIP expression via demethylation of HHIP gene and reduced the leukemia-supporting activity of AML/MDS-associated stromal cells. This effect of 5-aza-dC was negated by HHIP shRNA transfer into stromal cells. These results indicate that suppression of stromal HHIP expression could be involved in the progression of AML/MDS and 5-aza-dC may improve the protective function of BM stromal cells for AML/MDS. Disclosures: No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

13

SUBRAMANIAN, ABHISHEK, and RAM RUP SARKAR. "DYNAMICS OF GLI REGULATION AND A STRATEGY TO CONTROL CANCEROUS SITUATION: HEDGEHOG SIGNALING PATHWAY REVISITED." Journal of Biological Systems 23, no. 04 (November 30, 2015): 1550033. http://dx.doi.org/10.1142/s0218339015500333.

Full text

Abstract:

The hedgehog signaling cascade generates highly diverse, fine-tuned responses in response to the external stimulus by the sonic hedgehog (SHH) protein. This is required for the flawless functioning of the cell, its development, survival and proliferation; maintained through production of Glioma protein (GLI) and transcriptional activation of its target genes. Any change in the behavior of GLI response by ectopic expression of SHH or mutations in the core pathway components may cause serious consequences in the cell fate through rapid, uncontrolled and elevated production of GLI. Here, we present a simple but extensive computational model that considers the detailed reaction mechanisms involved in the hedgehog signal transduction and provides a detailed insight into regulation of GLI. For the first time, by explicit involvement of suppressor of fused (SUFU) and Hedgehog interacting protein (HHIP) reaction kinetics in the model, we try to demonstrate the vital importance of HHIP and SUFU in maintaining the graded response of GLI in response to SHH. By performing parameter variations, we capture the conversion of a graded response of GLI to an ultrasensitive switch under SUFU-deficient conditions that might predispose abnormal embryonic development and the irreversible switching response of GLI that corresponds to signal-independent pathway activation observed in cancers.

APA, Harvard, Vancouver, ISO, and other styles

14

Martin, S. T., N. Sato, S. Dhara, R. Chang, Steven R. Hustinx, T. Abe, Anirban Maitra, and Michael Goggins. "Aberrant methylation of the human hedgehog interacting protein (HHIP) gene in pancreatic neoplasms." Cancer Biology & Therapy 4, no. 7 (July 2005): 728–33. http://dx.doi.org/10.4161/cbt.4.7.1802.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Lin, Hung, Chen, Cheng, Li, Lin, Chang, Wu, and Ou. "Elevated Hedgehog-Interacting Protein Levels in Subjects with Prediabetes and Type 2 Diabetes." Journal of Clinical Medicine 8, no. 10 (October 6, 2019): 1635. http://dx.doi.org/10.3390/jcm8101635.

Full text

Abstract:

Background: The prevalence of diabetes is rapidly increasing worldwide and is highly associated with the incidence of cancers. In order to prevent diabetes, early diagnosis of prediabetes is important. However, biomarkers for prediabetes diagnosis are still scarce. The hedgehog-interacting protein (Hhip) is important in embryogenesis and is known to be a biomarker of several cancers. However, Hhip levels in subjects with diabetes are still unknown. Methods: In total, 314 participants were enrolled and divided into normal glucose tolerance (NGT; n = 75), impaired fasting glucose (IFG; n = 66), impaired glucose tolerance (IGT; n = 86), and newly diagnosed diabetes (NDD; n = 87) groups. Plasma Hhip levels were determined by an ELISA. The association between the Hhip and the presence of diabetes was examined by a multivariate linear regression analysis. Results: There were significant differences in the body mass index, systolic and diastolic blood pressure, fasting plasma glucose (FPG), post-load 2-h glucose, hemoglobin A1c (A1C), C-reactive protein, total cholesterol, triglyceride, and high- and low-density lipoprotein cholesterol levels among the groups. Concentrations of the Hhip were 2.45 ± 2.12, 4.40 ± 3.22, 4.44 ± 3.64, and 6.31 ± 5.35 ng/mL in subjects in the NGT, IFG, IGT, and NDD groups, respectively. In addition, we found that A1C and FPG were independently associated with Hhip concentrations. Using NGT as a reference group, IFG, IGT, and NDD were all independently associated with Hhip concentrations. Conclusions: Hhip was positively associated with prediabetes and type 2 diabetes mellitus.

APA, Harvard, Vancouver, ISO, and other styles

16

Lahmar, M. Z., E. Ahmed, I. Vachier, A. Fort, G. Marin, N. Molinari, A. Bergougnoux, and A. Bourdin. "Hedgehog Interacting Protein (HHIP) polymorphisms involved in early chronic obstructive pulmonary disease (COPD)." Revue des Maladies Respiratoires 39, no. 2 (February 2022): 115. http://dx.doi.org/10.1016/j.rmr.2022.02.017.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Bak, M., C. Hansen, K. Friis Henriksen, and N. Tommerup. "The human hedgehog-interacting protein gene: Structure and chromosome mapping to 4q31.21→q31.3." Cytogenetic and Genome Research 92, no. 3-4 (2001): 300–303. http://dx.doi.org/10.1159/000056918.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Miyata, Kana N., Xin-Ping Zhao, Shiao-Ying Chang, Min-Chun Liao, Chao-Sheng Lo, Isabelle Chenier, Jean Ethier, et al. "Increased urinary excretion of hedgehog interacting protein (uHhip) in early diabetic kidney disease." Translational Research 217 (March 2020): 1–10. http://dx.doi.org/10.1016/j.trsl.2019.11.001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Noguchi, Tatsuro, Kentaro Nakamura, Yuuki Satoda, Yohei Katoh, and Kazuhisa Nakayama. "CCRK/CDK20 regulates ciliary retrograde protein trafficking via interacting with BROMI/TBC1D32." PLOS ONE 16, no. 10 (October 8, 2021): e0258497. http://dx.doi.org/10.1371/journal.pone.0258497.

Full text

Abstract:

CCRK/CDK20 was reported to interact with BROMI/TBC1D32 and regulate ciliary Hedgehog signaling. In various organisms, mutations in the orthologs of CCRK and those of the kinase ICK/CILK1, which is phosphorylated by CCRK, are known to result in cilia elongation. Furthermore, we recently showed that ICK regulates retrograde ciliary protein trafficking and/or the turnaround event at the ciliary tips, and that its mutations result in the elimination of intraflagellar transport (IFT) proteins that have overaccumulated at the bulged ciliary tips as extracellular vesicles, in addition to cilia elongation. However, how these proteins cooperate to regulate ciliary protein trafficking has remained unclear. We here show that the phenotypes of CCRK-knockout (KO) cells closely resemble those of ICK-KO cells; namely, the overaccumulation of IFT proteins at the bulged ciliary tips, which appear to be eliminated as extracellular vesicles, and the enrichment of GPR161 and Smoothened on the ciliary membrane. The abnormal phenotypes of CCRK-KO cells were rescued by the exogenous expression of wild-type CCRK but not its kinase-dead mutant or a mutant defective in BROMI binding. These results together indicate that CCRK regulates the turnaround process at the ciliary tips in concert with BROMI and probably via activating ICK.

APA, Harvard, Vancouver, ISO, and other styles

20

Nchienzia, Henry, Min-Chun Liao, Xin-Ping Zhao, Shiao-Ying Chang, Chao-Sheng Lo, Isabelle Chenier, Julie Ingelfinger, John Chan, and Shao-Ling Zhang. "Role of Hedgehog Interacting Protein in High-Fat Diet-Mediated Pancreatic β-cell Dysfunction." Canadian Journal of Diabetes 42, no. 5 (October 2018): S54. http://dx.doi.org/10.1016/j.jcjd.2018.08.165.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Kleeff, J., H. Kayed, S. Keleg, N. Giese, M. W. Büchler, and H. Friess. "LOCALIZATION OF THE HUMAN HEDGEHOG-INTERACTING PROTEIN (HIP) IN THE NORMAL AND DISEASED PANCREAS." Pancreas 29, no. 4 (November 2004): 327. http://dx.doi.org/10.1097/00006676-200411000-00018.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Kayed, Hany, Jörg Kleeff, Irene Esposito, Thomas Giese, Shereen Keleg, Nathalia Giese, Markus W. Büchler, and Helmut Friess. "Localization of the human hedgehog-interacting protein (Hip) in the normal and diseased pancreas." Molecular Carcinogenesis 42, no. 4 (March 7, 2005): 183–92. http://dx.doi.org/10.1002/mc.20088.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Angot, E., K. Loulier, E. Traiffort, and M. Ruat. "[P4]: Analysis of cell proliferation in the mouse brain upon the adenovirus‐mediated transfer of sonic hedgehog and hedgehog interacting protein." International Journal of Developmental Neuroscience 24, no. 8 (November 16, 2006): 496–97. http://dx.doi.org/10.1016/j.ijdevneu.2006.09.068.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Enkhmandakh, Badam, Paul Robson, Pujan Joshi, Anushree Vijaykumar, Dong-Guk Shin, Mina Mina, and Dashzeveg Bayarsaihan. "Single-Cell Transcriptome Analysis Defines Expression of Kabuki Syndrome-Associated KMT2D Targets and Interacting Partners." Stem Cells International 2022 (August 12, 2022): 1–9. http://dx.doi.org/10.1155/2022/4969441.

Full text

Abstract:

Objectives. Kabuki syndrome (KS) is a rare genetic disorder characterized by developmental delay, retarded growth, and cardiac, gastrointestinal, neurocognitive, renal, craniofacial, dental, and skeletal defects. KS is caused by mutations in the genes encoding histone H3 lysine 4 methyltransferase (KMT2D) and histone H3 lysine 27 demethylase (KDM6A), which are core components of the complex of proteins associated with histone H3 lysine 4 methyltransferase SET1 (SET1/COMPASS). Using single-cell RNA data, we examined the expression profiles of Kmt2d and Kdm6a in the mouse dental pulp. In the incisor pulp, Kmt2d and Kdm6a colocalize with other genes of the SET1/COMPASS complex comprised of the WD-repeat protein 5 gene (Wdr5), the retinoblastoma-binding protein 5 gene (Rbbp5), absent, small, and homeotic 2-like protein-encoding gene (Ash2l), nuclear receptor cofactor 6 gene (Ncoa6), and Pax-interacting protein 1 gene (Ptip1). In addition, we found that Kmt2d and Kdm6a coexpress with the downstream target genes of the Wingless and Integrated (WNT) and sonic hedgehog signaling pathways in mesenchymal stem/stromal cells (MSCs) at different stages of osteogenic differentiation. Taken together, our results suggest an essential role of KMT2D and KDK6A in directing lineage-specific gene expression during differentiation of MSCs.

APA, Harvard, Vancouver, ISO, and other styles

25

Sun, Hui, Shu juan Ni, Min Ye, Weiwei Weng, Qiongyan Zhang, Meng Zhang, Cong Tan, et al. "Hedgehog Interacting Protein 1 is a Prognostic Marker and Suppresses Cell Metastasis in Gastric Cancer." Journal of Cancer 9, no. 24 (2018): 4642–49. http://dx.doi.org/10.7150/jca.27686.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Lao, Taotao, Kimberly Glass, Weiliang Qiu, Francesca Polverino, Kushagra Gupta, Jarrett Morrow, John Mancini, et al. "Haploinsufficiency of Hedgehog interacting protein causes increased emphysema induced by cigarette smoke through network rewiring." Genome Medicine 7, no. 1 (2015): 12. http://dx.doi.org/10.1186/s13073-015-0137-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Angeloni, Nicholas L., Christopher W. Bond, Diana Monsivais, Yi Tang, and Carol A. Podlasek. "The Role of Hedgehog-Interacting Protein in Maintaining Cavernous Nerve Integrity and Adult Penile Morphology." Journal of Sexual Medicine 6, no. 9 (September 2009): 2480–93. http://dx.doi.org/10.1111/j.1743-6109.2009.01349.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Yamamoto, Hiroyuki, Hiroaki Taniguchi, Nobuki Miyamoto, Chie Miyamoto, Tadateru Maehata, Katsuhiko Nosho, Kentaro Yamashita, et al. "S1644 Epigenetic Downregulation of the Hedgehog Interacting Protein Gene Is Frequently Involved in Gastrointestinal Tumorigenesis." Gastroenterology 134, no. 4 (April 2008): A—241. http://dx.doi.org/10.1016/s0016-5085(08)61115-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Cornesse, Yvonne, Tomas Pieler, and Thomas Hollemann. "Olfactory and lens placode formation is controlled by the hedgehog-interacting protein (Xhip) in Xenopus." Developmental Biology 277, no. 2 (January 2005): 296–315. http://dx.doi.org/10.1016/j.ydbio.2004.09.016.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Zhou, Xiaobo, Weiliang Qiu, J. Fah Sathirapongsasuti, Michael H. Cho, John D. Mancini, Taotao Lao, Derek M. Thibault, et al. "Gene expression analysis uncovers novel hedgehog interacting protein (HHIP) effects in human bronchial epithelial cells." Genomics 101, no. 5 (May 2013): 263–72. http://dx.doi.org/10.1016/j.ygeno.2013.02.010.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Shahi, Mehdi H., Idoya Zazpe, Mohammad Afzal, Subrata Sinha, Robert B. Rebhun, Bárbara Meléndez, Juan A. Rey, and Javier S. Castresana. "Epigenetic regulation of human hedgehog interacting protein in glioma cell lines and primary tumor samples." Tumor Biology 36, no. 4 (November 22, 2014): 2383–91. http://dx.doi.org/10.1007/s13277-014-2846-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Tada, Motohisa, Fumihiko Kanai, Yasuo Tanaka, Keisuke Tateishi, Miki Ohta, Yoshinari Asaoka, Motoko Seto, et al. "Down-Regulation of Hedgehog-Interacting Protein through Genetic and Epigenetic Alterations in Human Hepatocellular Carcinoma." Clinical Cancer Research 14, no. 12 (June 15, 2008): 3768–76. http://dx.doi.org/10.1158/1078-0432.ccr-07-1181.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Zhao, Xin-Ping, Min-Chun Liao, Shiao-Ying Chang, Shaaban Abdo, Yessoufou Aliou, Isabelle Chenier, Julie R. Ingelfinger, and Shao-Ling Zhang. "Maternal diabetes modulates kidney formation in murine progeny: the role of hedgehog interacting protein (HHIP)." Diabetologia 57, no. 9 (June 24, 2014): 1986–96. http://dx.doi.org/10.1007/s00125-014-3297-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Giakoustidis, Alexandros, Dimitrios Giakoustidis, Satvinder Mudan, Argyrios Sklavos, and Roger Williams. "Molecular Signalling in Hepatocellular Carcinoma: Role of and Crosstalk among Wnt/β-Catenin, Sonic Hedgehog, Notch and Dickkopf-1." Canadian Journal of Gastroenterology and Hepatology 29, no. 4 (2015): 209–17. http://dx.doi.org/10.1155/2015/172356.

Full text

Abstract:

Hepatocellular carcinoma is the sixth most common cancer worldwide. In the majority of cases, there is evidence of existing chronic liver disease from a variety of causes including viral hepatitis B and C, alcoholic liver disease and nonalcoholic steatohepatitis. Identification of the signalling pathways used by hepatocellular carcinoma cells to proliferate, invade or metastasize is of paramount importance in the discovery and implementation of successfully targeted therapies. Activation of Wnt/β-catenin, Notch and Hedgehog pathways play a critical role in regulating liver cell proliferation during development and in controlling crucial functions of the adult liver in the initiation and progression of human cancers. β-catenin was identified as a protein interacting with the cell adhesion molecule E-cadherin at the cell-cell junction, and has been shown to be one of the most important mediators of the Wnt signalling pathway in tumourigenesis. Investigations into the role of Dikkopf-1 in hepatocellular carcinoma have demonstrated controversial results, with a decreased expression of Dickkopf-1 and soluble frizzled-related protein in various cancers on one hand, and as a possible negative prognostic indicator of hepatocellular carcinoma on the other. In the present review, the authors focus on the Wnt/β-catenin, Notch and Sonic Hedgehog pathways, and their interaction with Dikkopf-1 in hepatocellular carcinoma.

APA, Harvard, Vancouver, ISO, and other styles

35

Sagar, G. D. Vivek, Balázs Gereben, Isabelle Callebaut, Jean-Paul Mornon, Anikó Zeöld, Wagner S. da Silva, Cristina Luongo, et al. "Ubiquitination-Induced Conformational Change within the Deiodinase Dimer Is a Switch Regulating Enzyme Activity." Molecular and Cellular Biology 27, no. 13 (April 23, 2007): 4774–83. http://dx.doi.org/10.1128/mcb.00283-07.

Full text

Abstract:

ABSTRACT Ubiquitination is a critical posttranslational regulator of protein stability and/or subcellular localization. Here we show that ubiquitination can also regulate proteins by transiently inactivating enzymatic function through conformational change in a dimeric enzyme, which can be reversed upon deubiquitination. Our model system is the thyroid hormone-activating type 2 deiodinase (D2), an endoplasmic reticulum-resident type 1 integral membrane enzyme. D2 exists as a homodimer maintained by interacting surfaces at its transmembrane and globular cytosolic domains. The D2 dimer associates with the Hedgehog-inducible ubiquitin ligase WSB-1, the ubiquitin conjugase UBC-7, and VDU-1, a D2-specific deubiquitinase. Upon binding of T4, its natural substrate, D2 is ubiquitinated, which inactivates the enzyme by interfering with D2's globular interacting surfaces that are critical for dimerization and catalytic activity. This state of transient inactivity and change in dimer conformation persists until deubiquitination. The continuous association of D2 with this regulatory protein complex supports rapid cycles of deiodination, conjugation to ubiquitin, and enzyme reactivation by deubiquitination, allowing tight control of thyroid hormone action.

APA, Harvard, Vancouver, ISO, and other styles

36

Treier, M., S. O'Connell, A. Gleiberman, J. Price, D. P. Szeto, R. Burgess, P. T. Chuang, A. P. McMahon, and M. G. Rosenfeld. "Hedgehog signaling is required for pituitary gland development." Development 128, no. 3 (February 1, 2001): 377–86. http://dx.doi.org/10.1242/dev.128.3.377.

Full text

Abstract:

Pituitary gland development serves as an excellent model system in which to study the emergence of distinct cell types from a common primordium in mammalian organogenesis. We have investigated the role of the morphogen Sonic hedgehog (SHH) in outgrowth and differentiation of the pituitary gland using loss- and gain-of-function studies in transgenic mice. Shh is expressed throughout the ventral diencephalon and the oral ectoderm, but its expression is subsequently absent from the nascent Rathke's pouch as soon as it becomes morphologically visible, creating a Shh boundary within the oral epithelium. We used oral ectoderm/Rathke's pouch-specific 5′ regulatory sequences (Pitx1(HS)) from the bicoid related pituitary homeobox gene (Pitx1) to target overexpression of the Hedgehog inhibitor Hip (Huntingtin interacting protein) to block Hedgehog signaling, finding that SHH is required for proliferation of the pituitary gland. In addition, we provide evidence that Hedgehog signaling, acting at the Shh boundary within the oral ectoderm, may exert a role in differentiation of ventral cell types (gonadotropes and thyrotropes) by inducing Bmp2 expression in Rathke's pouch, which subsequently regulates expression of ventral transcription factors, particularly Gata2. Furthermore, our data suggest that Hedgehog signaling, together with FGF8/10 signaling, synergizes to regulate expression of the LIM homeobox gene Lhx3, which has been proved to be essential for initial pituitary gland formation. Thus, SHH appears to exert effects on both proliferation and cell-type determination in pituitary gland development.

APA, Harvard, Vancouver, ISO, and other styles

37

Shahi, Mehdi H., Mohammad Afzal, Subrata Sinha, Charles G. Eberhart, Juan A. Rey, Xing Fan, and Javier S. Castresana. "Human hedgehog interacting protein expression and promoter methylation in medulloblastoma cell lines and primary tumor samples." Journal of Neuro-Oncology 103, no. 2 (September 19, 2010): 287–96. http://dx.doi.org/10.1007/s11060-010-0401-8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Taniguchi, H., H. Yamamoto, N. Akutsu, K. Nosho, Y. Adachi, K. Imai, and Y. Shinomura. "Transcriptional silencing of hedgehog-interacting protein by CpG hypermethylation and chromatic structure in human gastrointestinal cancer." Journal of Pathology 213, no. 2 (August 28, 2007): 131–39. http://dx.doi.org/10.1002/path.2216.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Liao, Min-Chun, Xin-Ping Zhao, Shiao-Ying Chang, Chao-Sheng Lo, Isabelle Chenier, Tomoko Takano, Julie R. Ingelfinger, and Shao-Ling Zhang. "AT2 R deficiency mediated podocyte loss via activation of ectopic hedgehog interacting protein (Hhip ) gene expression." Journal of Pathology 243, no. 3 (September 21, 2017): 279–93. http://dx.doi.org/10.1002/path.4946.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Holtz, Alexander M., Samuel C. Griffiths, Samantha J. Davis, Benjamin Bishop, Christian Siebold, and Benjamin L. Allen. "Secreted HHIP1 interacts with heparan sulfate and regulates Hedgehog ligand localization and function." Journal of Cell Biology 209, no. 5 (June 8, 2015): 739–58. http://dx.doi.org/10.1083/jcb.201411024.

Full text

Abstract:

Vertebrate Hedgehog (HH) signaling is controlled by several ligand-binding antagonists including Patched-1 (PTCH1), PTCH2, and HH-interacting protein 1 (HHIP1), whose collective action is essential for proper HH pathway activity. However, the molecular mechanisms used by these inhibitors remain poorly understood. In this paper, we investigated the mechanisms underlying HHIP1 antagonism of HH signaling. Strikingly, we found evidence that HHIP1 non–cell-autonomously inhibits HH-dependent neural progenitor patterning and proliferation. Furthermore, this non–cell-autonomous antagonism of HH signaling results from the secretion of HHIP1 that is modulated by cell type–specific interactions with heparan sulfate (HS). These interactions are mediated by an HS-binding motif in the cysteine-rich domain of HHIP1 that is required for its localization to the neuroepithelial basement membrane (BM) to effectively antagonize HH pathway function. Our data also suggest that endogenous, secreted HHIP1 localization to HS-containing BMs regulates HH ligand distribution. Overall, the secreted activity of HHIP1 represents a novel mechanism to regulate HH ligand localization and function during embryogenesis.

APA, Harvard, Vancouver, ISO, and other styles

41

Nie, Di-min, Qiu-ling Wu, Peng Zheng, Ping Chen, Ran Zhang, Bei-bei Li, Jun Fang, Ling-hui Xia, and Mei Hong. "Endothelial microparticles carrying hedgehog-interacting protein induce continuous endothelial damage in the pathogenesis of acute graft-versus-host disease." American Journal of Physiology-Cell Physiology 310, no. 10 (May 15, 2016): C821—C835. http://dx.doi.org/10.1152/ajpcell.00372.2015.

Full text

Abstract:

Accumulating evidence suggests that endothelial microparticles (EMPs), a marker of endothelial damage, are elevated in acute graft-versus-host disease (aGVHD), and that endothelial damage is implicated in the pathogenesis of aGVHD, but the mechanisms remain elusive. In this study, we detected the plasma EMP levels and endothelial damage in patients and mice with aGVHD in vivo and then examined the effects of EMPs derived from injured endothelial cells (ECs) on endothelial damage and the role of hedgehog-interacting protein (HHIP) carried by EMPs in these effects in vitro. Our results showed that EMPs were persistently increased in the early posttransplantation phase in patients and mice with aGVHD. Meanwhile, endothelial damage was continuous in aGVHD mice, but was temporary in non-aGVHD mice after transplantation. In vitro, EMPs induced endothelial damage, including increased EC apoptosis, enhanced reactive oxygen species, decreased nitric oxide production and impaired angiogenic activity. Enhanced expression of HHIP, an antagonist for the Sonic hedgehog (SHH) signaling pathway, was observed in patients and mice with aGVHD and EMPs from injured ECs. The endothelial damage induced by EMPs was reversed when the HHIP incorporated into EMPs was silenced with an HHIP small interfering RNA or inhibited with the SHH pathway agonist, Smoothened agonist. This work supports a feasible vicious cycle in which EMPs generated during endothelial injury, in turn, aggravate endothelial damage by carrying HHIP into target ECs, contributing to the continuously deteriorating endothelial damage in the development of aGVHD. EMPs harboring HHIP would represent a potential therapeutic target for aGVHD.

APA, Harvard, Vancouver, ISO, and other styles

42

Shearer, Robert F., Kari-Anne Myrum Frikstad, Jessie McKenna, Rachael A. McCloy, Niantao Deng, Andrew Burgess, Trond Stokke, Sebastian Patzke, and Darren N. Saunders. "The E3 ubiquitin ligase UBR5 regulates centriolar satellite stability and primary cilia." Molecular Biology of the Cell 29, no. 13 (July 2018): 1542–54. http://dx.doi.org/10.1091/mbc.e17-04-0248.

Full text

Abstract:

Primary cilia are crucial for signal transduction in a variety of pathways, including hedgehog and Wnt. Disruption of primary cilia formation (ciliogenesis) is linked to numerous developmental disorders (known as ciliopathies) and diseases, including cancer. The ubiquitin–proteasome system (UPS) component UBR5 was previously identified as a putative positive regulator of ciliogenesis in a functional genomics screen. UBR5 is an E3 ubiquitin ligase that is frequently deregulated in tumors, but its biological role in cancer is largely uncharacterized, partly due to a lack of understanding of interacting proteins and pathways. We validated the effect of UBR5 depletion on primary cilia formation using a robust model of ciliogenesis, and identified CSPP1, a centrosomal and ciliary protein required for cilia formation, as a UBR5-interacting protein. We show that UBR5 ubiquitylates CSPP1, and that UBR5 is required for cytoplasmic organization of CSPP1-comprising centriolar satellites in centrosomal periphery, suggesting that UBR5-mediated ubiquitylation of CSPP1 or associated centriolar satellite constituents is one underlying requirement for cilia expression. Hence, we have established a key role for UBR5 in ciliogenesis that may have important implications in understanding cancer pathophysiology.

APA, Harvard, Vancouver, ISO, and other styles

43

Hasebe, Takashi, Mitsuko Kajita, Yun-Bo Shi, and Atsuko Ishizuya-Oka. "Thyroid hormone-up-regulated hedgehog interacting protein is involved in larval-to-adult intestinal remodeling by regulating sonic hedgehog signaling pathway in Xenopus laevis." Developmental Dynamics 237, no. 10 (September 24, 2008): 3006–15. http://dx.doi.org/10.1002/dvdy.21698.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Takamoto, Norio, Bihong Zhao, Sophia Y. Tsai, and Francesco J. DeMayo. "Identification of Indian Hedgehog as a Progesterone-Responsive Gene in the Murine Uterus." Molecular Endocrinology 16, no. 10 (October 1, 2002): 2338–48. http://dx.doi.org/10.1210/me.2001-0154.

Full text

Abstract:

Abstract Progesterone (P4) plays a central role in normal uterine function, from embryo implantation in endometrium to establishment and maintenance of uterine quiescence during pregnancy in the myometrium. Considering its diverse physiological effects on female reproductive function, rather little is known about downstream events of P4 action. Recent progress in differential screening technologies facilitated identification of such inducible genes. We used uteri of wild-type and progesterone receptor null mutant mice as a starting material and screened for differentially expressed genes by medium-density cDNA expression array. Here, we report that the expression of the morphogen, Indian hedgehog (Ihh), is rapidly stimulated by P4 in the mouse uterus. The level of Ihh mRNA is induced within 3 h, after a single administration of P4 to ovariectomized mice. The induced Ihh mRNA and protein were localized to the luminal and glandular epithelial compartment of the endometrium. During pseudopregnancy, the Ihh mRNA level was transiently increased in the preimplantation period and d 3 and d 4 post coitum and then decreased rapidly at d 5 post coitum. Furthermore, the expression profile of patched-1, hedgehog interacting protein-1, and chicken ovalbumin upstream promoter-transcription factor II, genes known to be in the hedgehog signaling pathway in other tissues, followed the expression pattern of Ihh during the periimplantation period. Our results suggested that Ihh is regulated by P4, and the Ihh signaling axis may play a role in the preparation of the uterus for implantation during the periimplantation period.

APA, Harvard, Vancouver, ISO, and other styles

45

Isono, Kyoichi, Kazumi Nemoto, Yuanyuan Li, Yuki Takada, Rie Suzuki, Motoya Katsuki, Akira Nakagawara, and Haruhiko Koseki. "Overlapping Roles for Homeodomain-Interacting Protein Kinases Hipk1 and Hipk2 in the Mediation of Cell Growth in Response to Morphogenetic and Genotoxic Signals." Molecular and Cellular Biology 26, no. 7 (April 1, 2006): 2758–71. http://dx.doi.org/10.1128/mcb.26.7.2758-2771.2006.

Full text

Abstract:

ABSTRACT Homeodomain-interacting protein kinase 1 (Hipk1), 2, and 3 genes encode evolutionarily conserved nuclear serine/threonine kinases, which were originally identified as interacting with homeodomain-containing proteins. Hipks have been repeatedly identified as interactors for a vast range of functional proteins, including not only transcriptional regulators and chromatin modifiers but also cytoplasmic signal transducers, transmembrane proteins, and the E2 component of SUMO ligase. Gain-of-function experiments using cultured cells indicate growth regulatory roles for Hipks on receipt of morphogenetic and genotoxic signals. However, Hipk1 and Hipk2 singly deficient mice were grossly normal, and this is expected to be due to a functional redundancy between Hipk1 and Hipk2. Therefore, we addressed the physiological roles of Hipk family proteins by using Hipk1 Hipk2 double mutants. Hipk1 Hipk2 double homozygotes are progressively lost between 9.5 and 12.5 days postcoitus and frequently fail to close the anterior neuropore and exhibit exencephaly. This is most likely due to defective proliferation in the neural fold and underlying paraxial mesoderm, particularly in the ventral region, which may be attributed to decreased responsiveness to Sonic hedgehog signals. The present study indicated the overlapping roles for Hipk1 and Hipk2 in mediating cell proliferation and apoptosis in response to morphogenetic and genotoxic signals during mouse development.

APA, Harvard, Vancouver, ISO, and other styles

46

Chou, Hsuan-Wen, Hao-Chang Hung, Ching-Han Lin, An-Chi Lin, Ye-Fong Du, Kai-Pi Cheng, Chung-Hao Li, Chih-Jen Chang, Hung-Tsung Wu, and Horng-Yih Ou. "The Serum Concentrations of Hedgehog-Interacting Protein, a Novel Biomarker, Were Decreased in Overweight or Obese Subjects." Journal of Clinical Medicine 10, no. 4 (February 12, 2021): 742. http://dx.doi.org/10.3390/jcm10040742.

Full text

Abstract:

Although it was known that obesity is an independent risk factor for metabolic disorders including diabetes, the factors that link these diseases were obscure. The Hedgehog-interacting protein (Hhip) is a negative regulator in tissue remodeling, and inhibits the proliferation of adipocytes, and promotes their differentiation. In addition, Hhip was positively associated with diabetes. However, the relationship between Hhip and obesity in the human body remains unclear. An analysis of the relationship between Hhip and normal weight, overweight, and obesity levels. Participants receiving a physical checkup were recruited. Anthropometric and biochemical data were collected. Serum Hhip levels were determined by enzyme-linked immunosorbent assay (ELISA). Subjects were classified into normal-weight, overweight, and obese groups based on their body mass index (BMI). The association between Hhip and obesity was examined by multivariate linear regression analysis. In total, 294 subjects who were either of a normal weight (n = 166), overweight (n = 90), or obese (n = 38) were enrolled. Hhip concentrations were 6.51 ± 4.86 ng/mL, 5.79 ± 4.33 ng/mL, and 3.97 ± 3.4 ng/mL in normal-weight, overweight, and obese groups, respectively (p for trend = 0.032). Moreover, the regression analysis showed that BMI (β = −0.144, 95% confidence interval (CI) = −0.397−0.046, p = 0.013) was negatively associated with Hhip concentrations after adjusting for sex and age. Being overweight (β = −0.181, 95% CI = −3.311−0.400, p = 0.013) and obese (β = −0.311, 95% CI = −6.393−2.384, p < 0.001) were independently associated with Hhip concentrations after adjusting for sex, age, fasting plasma glucose, the insulin level, and other cardiometabolic risk factors. Our results showed that overweight and obese subjects had lower Hhip concentrations than those of normal weight. Being overweight and obese were negatively associated with Hhip concentrations. Hhip might be a link between obesity and diabetes.

APA, Harvard, Vancouver, ISO, and other styles

47

Lee, Woo, Seul Lee, Seung Yim, Daham Kim, Hyunji Kim, Seonhyang Jeong, Sang Jung, Young Jo, and Jandee Lee. "Whole Exome Sequencing Identifies a Novel Hedgehog-Interacting Protein G516R Mutation in Locally Advanced Papillary Thyroid Cancer." International Journal of Molecular Sciences 19, no. 10 (September 21, 2018): 2867. http://dx.doi.org/10.3390/ijms19102867.

Full text

Abstract:

Locally advanced thyroid cancer exhibits aggressive clinical features requiring extensive neck dissection. Therefore, it is important to identify changes in the tumor biology before local progression. Here, whole exome sequencing (WES) using tissues from locally advanced papillary thyroid cancer (PTC) presented a large number of single nucleotide variants (SNVs) in the metastatic lymph node (MLN), but not in normal tissues and primary tumors. Among those MLN-specific SNVs, a novel HHIP G516R (G1546A) mutation was also observed. Interestingly, in-depth analysis for exome sequencing data from the primary tumor presented altered nucleotide ‘A’ at a very low frequency indicating intra-tumor heterogeneity between the primary tumor and MLN. Computational prediction models such as PROVEAN and Polyphen suggested that HHIP G516R might affect protein function and stability. In vitro, HHIP G516R increased cell proliferation and promoted cell migration in thyroid cancer cells. HHIP G516R, a missense mutation, could be a representative example for the intra-tumor heterogeneity of locally advanced thyroid cancer, which can be a potential future therapeutic target for this disease.

APA, Harvard, Vancouver, ISO, and other styles

48

Loulier, Karine, Martial Ruat, and Elisabeth Traiffort. "Analysis of hedgehog interacting protein in the brain and its expression in nitric oxide synthase-positive cells." NeuroReport 16, no. 17 (November 2005): 1959–62. http://dx.doi.org/10.1097/01.wnr.0000187632.91375.81.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Mosimann, Christian, George Hausmann, and Konrad Basler. "The role of Parafibromin/Hyrax as a nuclear Gli/Ci-interacting protein in Hedgehog target gene control." Mechanisms of Development 126, no. 5-6 (May 2009): 394–405. http://dx.doi.org/10.1016/j.mod.2009.02.002.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

PACES-FESSY, Mélanie, Dominique BOUCHER, Emile PETIT, Sandrine PAUTE-BRIAND, and Marie-Françoise BLANCHET-TOURNIER. "The negative regulator of Gli, Suppressor of fused (Sufu), interacts with SAP18, Galectin3 and other nuclear proteins." Biochemical Journal 378, no. 2 (March 1, 2004): 353–62. http://dx.doi.org/10.1042/bj20030786.

Full text

Abstract:

Sufu (Suppressor of fused) is a negative regulator of the Hedgehog signal-transduction pathway, interacting directly with the Gli family of transcription factors. However, its function remains poorly understood. In the present study, we determined the expression, tissue distribution and biochemical properties of mSufu (mouse Sufu) protein. We identified several mSufu variants of which some were phosphorylated. A yeast two-hybrid screen with mSufu as bait allowed us to identify several nuclear proteins as potential partners of mSufu. Most of these partners, such as SAP18 (Sin3-associated polypeptide 18), pCIP (p300/CBP-cointegrator protein) and PIAS1 (protein inhibitor of activated signal transduction and activators of transcription 1), are involved in either repression or activation of transcription and two of them, Galectin3 and hnRNPA1 (heterogeneous nuclear ribonucleoprotein A1), have a nuclear function in pre-mRNA splicing. We confirmed the mSufu–SAP18 and mSufu–Galectin3 interactions by independent biochemical assays. Using a cell transfection assay, we also demonstrated that mSufu protein (484 amino acids) is predominantly cytoplasmic but becomes mostly nuclear when a putative nuclear export signal is mutated or after treatment of the cells with leptomycin B. Moreover, mSufu is translocated to the nucleus when co-expressed with SAP18, which is normally found in this compartment. In contrast, Galectin3 is translocated to the cytoplasm when it is co-expressed with mSufu. Our findings indicate that mSufu is a shuttle protein that appears to be extremely versatile in its ability to bind different proteins in both the cytoplasm and nucleus.

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!