Serine Protease Activity of Calnuc

Kanuru, Madhavi; Raman, Rajeev; Aradhyam, Gopala Krishna

doi:10.1074/jbc.m112.382846

Cited by 13 publications

(9 citation statements)

References 41 publications

(49 reference statements)

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“…8 C and D) had higher deuterium uptake after the addition of Zn 2+ , indicating the increased solvent accessibility of these regions. Notably, a change in the HDX level of Nucb2s occurred in the region of the putative Zn 2+ -binding site HFREX n H [48] . For hsNucb2, the major HDX differences between apo- and Zn 2+ -hsNucb2 were prominent at early time points: 10 s and 1 min (data not shown).…”

Section: Resultsmentioning

confidence: 99%

“…The interaction between Ca 2+ and Nucb2s resulted in a disorder-to-order transition and dimerization of both proteins [49] . In the structure of Nucb2s, two EF-hand domains are present, which are responsible for Ca 2+ /Mg 2+ binding [6] and one putative motif of Zn 2+ -binding [48] . In this study, we determined the thermodynamic properties of Nucb2s interacting with Mg 2+ and Zn 2+ , as well as their influence on the structure of Nucb2s.…”

Section: Discussionmentioning

confidence: 99%

“…Nucb2 possesses two EF-hand domains [37] , which are able to bind Ca 2+ and Mg 2+ ions [6] . Additionally, Nucb2 contains a putative Zn 2+ -binding motif at its N-terminal half, similar to its paralogue Nucb1 [48] . Our previous research showed that Nucb2s from Gallus gallus (ggNucb2) and Homo sapiens (hsNucb2) belong to the family of intrinsically disordered proteins (IDPs) [49] .…”

Section: Introductionmentioning

confidence: 99%

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Nucleobindin-2 consists of two structural components: The Zn2+-sensitive N-terminal half, consisting of nesfatin-1 and -2, and the Ca2+-sensitive C-terminal half, consisting of nesfatin-3

Bystranowska

Skorupska

Sołtys

et al. 2021

Computational and Structural Biotechnology Journal

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Nucleobindin-2 consists of two structural components: The Zn2+-sensitive N-terminal half, consisting of nesfatin-1 and -2, and the Ca2+-sensitive C-terminal half, consisting of nesfatin-3

Bystranowska

Skorupska

Sołtys

et al. 2021

Computational and Structural Biotechnology Journal

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show abstract

“…62 Expression of APOA1 was significantly reduced in HCV-related tumors from clinical studies when compared to paired, non-tumorous tissues. 63 NUCB1 is a multifunctional protein that regulates cell signaling 64 and the unfolded protein response. 65 It interacted with NS5B in this screen, but was found to interact with HCV GT1a NS5A in an earlier study.…”

Section: Discussionmentioning

confidence: 99%

Identification and comparative analysis of hepatitis C virus–host cell protein interactions

et al. 2013

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Hepatitis C virus (HCV) alters the global behavior of the host cell to create an environment conducive to its own replication, but much remains unknown about how HCV proteins elicit these changes. Thus, a better understanding of the interface between the virus and host cell is required. Here we report the results of a large-scale yeast two-hybrid screen to identify protein-protein interactions between HCV genotype 2a (strain JFH1) and cellular factors. Our study identified 112 unique interactions between 7 HCV and 94 human proteins, over 40% of which have been linked to HCV infection by other studies. These interactions develop a more complete picture of HCV infection, providing insight into HCV manipulation of pathways, such as lipid and cholesterol metabolism, that were previously linked to HCV infection and implicating novel targets within microtubule-organizing centers, the complement system and cell cycle regulatory machinery. In an effort to understand the relationship between HCV and related viruses, we compared the HCV 2a interactome to those of other HCV genotypes and to the related dengue virus. Greater overlap was observed between HCV and dengue virus targets than between HCV genotypes, demonstrating the value of parallel screening approaches when comparing virus-host cell interactomes. Using siRNAs to inhibit expression of cellular proteins, we found that five of the ten shared targets tested (CUL7, PCM1, RILPL2, RNASET2, and TCF7L2) were required for replication of both HCV and dengue virus. These shared interactions provide insight into common features of the viral life cycles of the family Flaviviridae.

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“…Interestingly, one member, nucleobindin 1 (NUCB1), has been shown to modulate the UPR via inhibition of ATF6 activity (Tsukumo et al, 2007 ). NUCB1 is a 63-kDa calcium-binding protein with multiple domains, including a leucine rich zipper, carboxypeptidase-like motifs, two zinc binding sites, and two EF-hands (Miura et al, 1992 , 1996 ; Wendel et al, 1995 ; Kanuru et al, 2013 ). The precise physiological and biochemical functions of NUCB1, however, are not well understood and whether NUCB1 plays a role in PDAC has not been explored.…”

Section: Introductionmentioning

confidence: 99%

NUCB1 Suppresses Growth and Shows Additive Effects With Gemcitabine in Pancreatic Ductal Adenocarcinoma via the Unfolded Protein Response

Hua

Zhang

Sheng

et al. 2021

Front. Cell Dev. Biol.

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Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with poor patient prognosis. A cellular stress response mechanism called the unfolded protein response (UPR) has been implicated in PDAC progression. More recently, nucleobindin 1 (NUCB1), a calcium-binding protein, has been shown to control the UPR but its precise role in PDAC has not been explored. Here, we found that downregulation of NUCB1 was associated with poor prognosis in patients with PDAC. Functionally, NUCB1 overexpression suppressed pancreatic cancer cell proliferation and showed additive effects with gemcitabine (GEM) in vitro and in vivo. Moreover, by controlling ATF6 activity, NUCB1 overexpression suppressed GEM-induced UPR and autophagy. Last but not least, we uncovered METTL3-mediated m6A modification on NUCB1 5′UTR via the reader YTHDF2 as a mechanism for NUCB1 downregulation in PDAC. Taken together, our study revealed crucial functions of NUCB1 in suppressing proliferation and enhancing the effects of gemcitabine in pancreatic cancer cells and identified METTL3-mediated m6A modification as a mechanism for NUCB1 downregulation in PDAC.

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Serine Protease Activity of Calnuc

Cited by 13 publications

References 41 publications

Nucleobindin-2 consists of two structural components: The Zn2+-sensitive N-terminal half, consisting of nesfatin-1 and -2, and the Ca2+-sensitive C-terminal half, consisting of nesfatin-3

Nucleobindin-2 consists of two structural components: The Zn2+-sensitive N-terminal half, consisting of nesfatin-1 and -2, and the Ca2+-sensitive C-terminal half, consisting of nesfatin-3

Identification and comparative analysis of hepatitis C virus–host cell protein interactions

NUCB1 Suppresses Growth and Shows Additive Effects With Gemcitabine in Pancreatic Ductal Adenocarcinoma via the Unfolded Protein Response

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