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Artículos de revistas sobre el tema "Cs41"

Autor: Grafiati
Publicado: 26 de julio de 2024
Última modificación: 28 de julio de 2024

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1

Xia, Kai Sheng, and Qiu Ming Gao. "Synthesis and Hydrogen Adsorption Properties of Templated Nanoporous Carbons." Advanced Materials Research 239-242 (May 2011): 2116–19. http://dx.doi.org/10.4028/www.scientific.net/amr.239-242.2116.

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Four nanoporous carbons have been synthesized by using similar silica template method. The structural characterizations showed that the carbons retained ordered hexagonal or cubic pore structure expect for disordered CS41, which was prepared using MCM-41 as template. Nitrogen adsorptions at 77 K revealed that carbons with different pore size distribution, specific surface area and pore volume were obtained. The hydrogen adsorption capacity was measured by volumetric method, and the most promising candidate resulted to be microporous carbon CS41, which exhibited the highest H2uptake of 1.17 wt % at 77 K and 1 bar. The capacities of hydrogen adsorbed in the nanoporous carbons were correlated with specific surface area and microporous volume. The result demonstrated that the H2uptake in the carbons had essential relationship with volume of pores smaller than 1 nm.
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E Schulze, Kirsten, and Julie Chernov Hwang. "Militant Islam in Southeast Asia: New Insights into Jihad in Indonesia, Malaysia and the Philippines." Contemporary Southeast Asia 41, no. 1 (2019): 1–13. http://dx.doi.org/10.1355/cs41-1a.

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Hwang, Julie Chernov. "Dakwah before Jihad: Understanding the Behaviour of Jemaah Islamiyah." Contemporary Southeast Asia 41, no. 1 (2019): 14–34. http://dx.doi.org/10.1355/cs41-1b.

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E Schulze, Kirsten. "From Ambon to Poso: Comparative and Evolutionary Aspects of Local Jihad in Indonesia." Contemporary Southeast Asia 41, no. 1 (2019): 35–62. http://dx.doi.org/10.1355/cs41-1c.

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Fealy, Greg. "Apocalyptic Thought, Conspiracism and Jihad in Indonesia." Contemporary Southeast Asia 41, no. 1 (2019): 63–85. http://dx.doi.org/10.1355/cs41-1d.

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6

Chinyong Liow, Joseph, and Aida Arosoaie. "The Sound of Silence: Nuancing Religiopolitical Legitimacy and Conceptualizing the Appeal of ISIS in Malaysia." Contemporary Southeast Asia 41, no. 1 (2019): 86–113. http://dx.doi.org/10.1355/cs41-1e.

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Temby, Quinton. "Cells, Factions and Suicide Operatives: The Fragmentation of Militant Islamism in the Philippines Post-Marawi." Contemporary Southeast Asia 41, no. 1 (2019): 114–37. http://dx.doi.org/10.1355/cs41-1f.

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Hearman, Vannessa, and Annie Pohlman. "Unmarked Graves: Death and Survival in the Anti-Communist Violence in East Java, Indonesia." Contemporary Southeast Asia 41, no. 1 (2019): 138–40. http://dx.doi.org/10.1355/cs41-1g.

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Hawksley, Humphrey, and Hoang Thi Ha. "Asian Waters: The Struggle Over the South China Sea and the Strategy of Chinese Expansion." Contemporary Southeast Asia 41, no. 1 (2019): 141–43. http://dx.doi.org/10.1355/cs41-1h.

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Crouch, Melissa, and Andrew Harding. "The Business of Transition: Law Reform, Development and Economics in Myanmar." Contemporary Southeast Asia 41, no. 1 (2019): 144–46. http://dx.doi.org/10.1355/cs41-1i.

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M. Smith, Jeff, and Jim Rolfe. "Asia's Quest for Balance: China's Rise and Balancing in the Indo-Pacific." Contemporary Southeast Asia 41, no. 1 (2019): 147–49. http://dx.doi.org/10.1355/cs41-1j.

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12

Eyler, Brian, and Pichamon Yeophantong. "Last Days of the Mighty Mekong." Contemporary Southeast Asia 41, no. 1 (2019): 150–52. http://dx.doi.org/10.1355/cs41-1k.

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McCargo, Duncan, Prajak Kongkirati, Anyarat Chattharakul, et al. "Roundtable: Thailand’s Amazing 24 March 2019 Elections." Contemporary Southeast Asia 41, no. 2 (2018): 153–222. http://dx.doi.org/10.1355/cs41-2a.

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14

Thi Ha, Hoang. "Understanding China’s Proposal for an ASEAN-China Community of Common Destiny and ASEAN’s Ambivalent Response." Contemporary Southeast Asia 41, no. 2 (2018): 223–54. http://dx.doi.org/10.1355/cs41-2j.

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15

Warburton, Eve, and Edward Aspinall. "Explaining Indonesia’s Democratic Regression: Structure, Agency and Popular Opinion." Contemporary Southeast Asia 41, no. 2 (2018): 255–85. http://dx.doi.org/10.1355/cs41-2k.

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Koga, Kei. "Japan’s “Free and Open Indo-Pacific” Strategy: Tokyo’s Tactical Hedging and the Implications for ASEAN." Contemporary Southeast Asia 41, no. 2 (2018): 286–313. http://dx.doi.org/10.1355/cs41-2l.

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S. Davidson, Jamie, and Michael Vatikiotis. "Indonesia: Twenty Years of Democracy." Contemporary Southeast Asia 41, no. 2 (2018): 314–16. http://dx.doi.org/10.1355/cs41-2m.

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18

Serena I. Diokno, Maria, Hsin-Huang Michael Hsiao, Alan H. Yang, and Xue Gong. "China’s Footprints in Southeast Asia." Contemporary Southeast Asia 41, no. 2 (2018): 317–19. http://dx.doi.org/10.1355/cs41-2n.

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19

Sachsenröder, Wolfgang, and Risa J Toha. "Power Broking in the Shade: Party Finances and Money Politics in Southeast Asia." Contemporary Southeast Asia 41, no. 2 (2018): 320–22. http://dx.doi.org/10.1355/cs41-2o.

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20

Croissant, Aurel, and Adhi Priamarizki. "Civil-Military Relations in Southeast Asia." Contemporary Southeast Asia 41, no. 2 (2018): 323–25. http://dx.doi.org/10.1355/cs41-2p.

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21

Un, Kheang, and Sivhuoch Ou. "Cambodia: Return to Authoritarianism." Contemporary Southeast Asia 41, no. 2 (2018): 326–28. http://dx.doi.org/10.1355/cs41-2q.

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22

Haacke, Jürgen, and John Harley Breen. "From Benign Neglect to Effective Re-engagement? Assessing British Strategizing and Policies Towards Southeast Asia Since 2010." Contemporary Southeast Asia 41, no. 3 (2020): 329–63. http://dx.doi.org/10.1355/cs41-3a.

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23

Efriandi, Tri, Oscar Couwenberg, and Ronald L. Holzhacker. "Decentralization and Public Service Provision:A case Study of the Education Sector in Jayawijaya District, Papua, Indonesia." Contemporary Southeast Asia 41, no. 3 (2020): 364–89. http://dx.doi.org/10.1355/cs41-3b.

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Sirivunnabood, Punchada. "The Rules Change but the Players Don’t: Factional Politics and Thailand’s March 2019 Elections." Contemporary Southeast Asia 41, no. 3 (2020): 390–417. http://dx.doi.org/10.1355/cs41-3c.

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Xue, Song. "Why Joint Development Agreements Fail: Implications for the South China Sea Dispute." Contemporary Southeast Asia 41, no. 3 (2020): 418–46. http://dx.doi.org/10.1355/cs41-3d.

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26

Negara, Siwage Dharma. "Book Reviews democracy for sale: Elections, Clientlism and the state in Indonesia. By Edward Aspinall and Ward Berenschot. Ithaca, New York: Cornell University Press, 2019). Softcover: 308pp." Contemporary Southeast Asia 41, no. 3 (2020): 447–49. http://dx.doi.org/10.1355/cs41-3e.

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27

Dewi, Sita. "Scandal & Democracy: Media Politics in Indonesia.By Mary E.McCoy. Ithaca, New York: Cornell, 2019. Softcover: 208pp." Contemporary Southeast Asia 41, no. 3 (2020): 450–52. http://dx.doi.org/10.1355/cs41-3f.

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28

T Tow, William. "Asia’s Regional Architecture: Alliances and Institutions in the Pacific Century. By Andrew Yeo. Stanford, California: Stanford University Press, 2019. Hardcover: 243pp." Contemporary Southeast Asia 41, no. 3 (2020): 453–55. http://dx.doi.org/10.1355/cs41-3g.

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29

Bradford, John. "Aristocracy of Armed Talent: The Military Elite in Singapore.By Sameul Ling Wei Chan.Singapore NUS Press,2019 softcover: 495pp." Contemporary Southeast Asia 41, no. 3 (2020): 456–59. http://dx.doi.org/10.1355/cs41-3h.

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Vasavakul, Thaveeporn Vasavakul. "Speaking Out in Vietnam: Public Political Criticism in a Communist Party-Ruled Nation . By Benedict J. Tria Kerkvliet. Ithaca: Cornell University Press, 2019. Hardcover: 224pp." Contemporary Southeast Asia 41, no. 3 (2020): 460–62. http://dx.doi.org/10.1355/cs41-3i.

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31

Le Thu, Huong. "China’s Asia: Triangular Dynamics since the Cold War. By Lowell Dittmer. Lanham, Maryland: Rowman & Littlefield, 2018. Softcover: 289pp." Contemporary Southeast Asia 41, no. 3 (2020): 463–65. http://dx.doi.org/10.1355/cs41-3j.

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32

Narine, Shaun. "ASEAN’s Half Century: A Political History of the Association of Southeast Asian Nations. By Donald E. Weatherbee. Lanhan, Maryland: Rowman and Littlefield, 2019. Softcover." Contemporary Southeast Asia 41, no. 3 (2020): 466–68. http://dx.doi.org/10.1355/cs41-3k.

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33

Ahammed, S., M. M. Hossain, M. Zakaria, B. Ahmed, and M. A. K. Mian. "Combining Ability and Gene Action in Cucumber (Cucumis Sativus L.)." Journal of Agricultural Studies 5, no. 4 (2018): 145. http://dx.doi.org/10.5296/jas.v6i2.13329.

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Combining ability and genetic components of eleven inbred line of cucumber were estimated following line x tester mating design for qualitative and quantitative characters. Three inbred lines were used as tester. Variance within the treatments, parents, parent vs crosses, crosses, testers and line x tester interaction were highly significant for all the characters. Considering the gca effects the lines CS08, CS16, CS040, CS07 and CS51 were best for their earliness and other horticulture traits. The hybrids CS07×CS08, CS16×CS44, CS51×CS44, CS40×CS08, CS17×CS39 were superior in terms of yield per plant and its component characters. The magnitude of σ2SCA was high in all characters compared to σ2GCA and dominance variance (σ2D) was higher than the additive genetic variance (σ2A) indicating that the predominance role of non-additive gene action. The results indicated the importance of heterosis breeding for effective utilization of non-additive genetic variance in cucumber.
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34

Teodori, Rosana Macher, Joice Betini, Larissa Salgado de Oliveira, Luciane Lobato Sobral, Sibele Yoko Mattozo Takeda, and Maria Imaculada de Lima Montebelo. "Swimming Exercise in the Acute or Late Phase after Sciatic Nerve Crush Accelerates Nerve Regeneration." Neural Plasticity 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/783901.

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There is no consensus about the best time to start exercise after peripheral nerve injury. We evaluated the morphological and functional characteristics of the sciatic nerves of rats that began to swim immediately after crush nerve injury (CS1), those that began to swim 14 days after injury (CS14), injured rats not submitted to swimming (C), and uninjured rats submitted to swimming (S). After 30 days the number of axons in CS1 and CS14 was lower than in C (P<0.01). The diameter of axons and nerve fibers was larger in CS1 (P<0.01) and CS14 (P<0.05) than in C, and myelin sheath thickness was lower in all crushed groups (P<0.05). There was no functional difference between CS1 and CS14 (P>0.05). Swimming exercise applied during the acute or late phase of nerve injury accelerated nerve regeneration and synaptic elimination after axonotmesis, suggesting that exercise may be initiated immediately after injury.
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35

Li, Siqi, Hyesuk Seo, Ipshita Upadhyay, and Weiping Zhang. "A Polyvalent Adhesin–Toxoid Multiepitope-Fusion-Antigen-Induced Functional Antibodies against Five Enterotoxigenic Escherichia coli Adhesins (CS7, CS12, CS14, CS17, and CS21) but Not Enterotoxins (LT and STa)." Microorganisms 11, no. 10 (2023): 2473. http://dx.doi.org/10.3390/microorganisms11102473.

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The increasing prevalence and association with moderate-to-severe diarrhea make enterotoxigenic Escherichia coli (ETEC) adhesins CS7, CS12, CS14, CS17, and CS21 potential targets of ETEC vaccines. Currently, there are no vaccines licensed to protect against ETEC, a top cause of children’s diarrhea and travelers’ diarrhea. Recently, a polyvalent adhesin protein (adhesin MEFA-II) was demonstrated to induce antibodies that inhibited adherence from these five ETEC adhesins and reduced the enterotoxicity of ETEC heat-stable toxin (STa), which plays a key role in causing ETEC-associated diarrhea. To improve adhesin MEFA-II for functional antibodies against STa toxin and the other ETEC toxin, heat-labile toxin (LT), we modified adhesin MEFA-II by adding another STa toxoid and an LT epitope; we examined the new antigen immunogenicity (to five adhesins and two toxins) and more importantly antibody functions against ETEC adherence and STa and LT enterotoxicity. Data show that mice intramuscularly immunized with the new antigen (adhesin MEFA-IIb) developed robust IgG responses to the targeted adhesins (CS7, CS12, CS14, CS17, and CS21) and toxins (STa and LT). Mouse antibodies inhibited the adherence of ETEC strains expressing any of these five adhesins but failed to neutralize STa or LT enterotoxicity. In further studies, rabbits intramuscularly immunized with adhesin MEFA-IIb developed robust antigen-specific antibodies; when challenged with an ETEC isolate expressing CS21 adhesin (JF2101, CS21, and STa), the immunized rabbits showed a significant reduction in intestinal colonization by ETEC bacteria. These data indicate that adhesin MEFA-IIb is broadly immunogenic and induces functional antibodies against the targeted ETEC adhesins but not the toxins.
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36

Walia, Sohan Singh, Subhash Babu, Roopinder Singh Gill, et al. "Designing Resource-Efficient and Environmentally Safe Cropping Systems for Sustainable Energy Use and Economic Returns in Indo-Gangetic Plains, India." Sustainability 14, no. 21 (2022): 14636. http://dx.doi.org/10.3390/su142114636.

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Achieving an economically feasible and environmentally robust model in agriculture while satisfying the expanding population’s food demands is a global challenge. Hence, a three-year (2014–2017) study was conducted at Punjab Agricultural University, Ludhiana to design environmentally clean, energy-efficient, and profitable cropping systems. Twelve cropping systems viz., rice-wheat (CS1), basmati rice-hayola (transplanted)-mung bean (CS2), basmati rice-radish-maize (CS3), maize-potato-maize (CS4), maize + turmeric-barley + linseed (CS5), maize + turmeric-wheat + linseed (CS6), maize + radish-wheat + linseed-mung bean (CS7), groundnut + pigeon pea (5:1)-wheat + sarson (9:1) (CS8), maize + black gram-pea (bed) + celery (furrows) (CS9),: maize + pigeon pea-chickpea (bed) + gobhi sarson (furrows) (CS10), maize (green cobs) + vegetable cowpea + dhaincha (Sesbania spp.)-chickpea + gobhi sarson (CS11) and sorghum + cowpea (fodder)-wheat + gobhi sarson (9:1) (CS12) were tested in a four-times-replicated randomized block design. CS11 had the maximum system productivity (28.57 Mg ha−1), production efficiency (78.27 Kg Day−1 ha−1), irrigation water use efficiency (2.38 kg m−3), system net returns (4413.3 US$ ha−1), and benefit to cost (B:C) ratio (2.83) over others. In comparison to the CS1 system, this cropping system required ~78% less irrigation water for a unit economic production. However, the cultivation of CS12 registered the highest energy use efficiency (49.06%), net energy returns (6.46 × 103 MJ ha⁻¹), and global warming potential (GWP) (Mg CO2 e ha−1) at spatial scale. Among all the intensified systems, CS11 had the lowest GHGI (0.29 kg CO2 e kg−1). Furthermore, cultivation of CS6 resulted in the maximum bacterial and actinomycetes population in the soil, while CS5 yielded the highest fungal count (23.8 × 103 cfu g−1 dry soil) in soil. Our study suggests that the cultivation of CS11 is a resource-efficient, economically viable, and environmentally clean production system and could be a potential alternative to rice-wheat systems for developing a green economy policy for agricultural development in the Indo-Gangetic Plains (IGP) of India.
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37

Anantha, Ravi P., Annette L. McVeigh, Lanfong H. Lee, et al. "Evolutionary and Functional Relationships of Colonization Factor Antigen I and Other Class 5 Adhesive Fimbriae of Enterotoxigenic Escherichia coli." Infection and Immunity 72, no. 12 (2004): 7190–201. http://dx.doi.org/10.1128/iai.72.12.7190-7201.2004.

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ABSTRACT Colonization factor antigen I (CFA/I) is the archetype of eight genetically related fimbriae of enterotoxigenic Escherichia coli (ETEC) designated class 5 fimbriae. Assembled by the alternate chaperone pathway, these organelles comprise a rigid stalk of polymerized major subunits and an apparently tip-localized minor adhesive subunit. We examined the evolutionary relationships of class 5-specific structural proteins and correlated these with functional properties. We sequenced the gene clusters encoding coli surface antigen 4 (CS4), CS14, CS17, CS19, and putative colonization factor antigen O71 (PCFO71) and analyzed the deduced proteins and the published homologs of CFA/I, CS1, and CS2. Multiple alignment and phylogenetic analysis of the proteins encoded by each operon define three subclasses, 5a (CFA/I, CS4, and CS14), 5b (CS1, CS17, CS19, and PCFO71), and 5c (CS2). These share distant evolutionary relatedness to fimbrial systems of three other genera. Subclass divisions generally correlate with distinguishing in vitro adherence phenotypes of strains bearing the ETEC fimbriae. Phylogenetic comparisons of the individual structural proteins demonstrated greater intrasubclass conservation among the minor subunits than the major subunits. To correlate this with functional attributes, we made antibodies against CFA/I and CS17 whole fimbriae and maltose-binding protein fusions with the amino-terminal half of the corresponding minor subunits. Anti-minor subunit Fab preparations showed hemagglutination inhibition (HAI) of ETEC expressing homologous and intrasubclass heterologous colonization factors while anti-fimbrial Fab fractions showed HAI activity limited to colonization factor-homologous ETEC. These results were corroborated with similar results from the Caco-2 cell adherence assay. Our findings suggest that the minor subunits of class 5 fimbriae may be superior to whole fimbriae in inducing antiadhesive immunity.
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Nandre, Rahul M., Xiaosai Ruan, Qiangde Duan, David A. Sack, and Weiping Zhang. "Antibodies derived from an enterotoxigenic Escherichia coli (ETEC) adhesin tip MEFA (multiepitope fusion antigen) against adherence of nine ETEC adhesins: CFA/I, CS1, CS2, CS3, CS4, CS5, CS6, CS21 and EtpA." Vaccine 34, no. 31 (2016): 3620–25. http://dx.doi.org/10.1016/j.vaccine.2016.04.003.

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Vilchez, Samuel, Sylvia Becker-Dreps, Erick Amaya, et al. "Characterization of enterotoxigenic Escherichia coli strains isolated from Nicaraguan children in hospital, primary care and community settings." Journal of Medical Microbiology 63, no. 5 (2014): 729–34. http://dx.doi.org/10.1099/jmm.0.066779-0.

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Enterotoxigenic Escherichia coli (ETEC) is one of the most common causes of diarrhoea among young children in developing countries. ETEC vaccines offer promise in reducing the burden of ETEC disease, but the development of these vaccines relies on the characterization of ETEC isolates from a variety of settings. To best reflect the full spectrum of ETEC disease in León, Nicaragua, the aim of this study was to characterize ETEC strains isolated from children with diarrhoea attending different settings (hospital, primary care clinics and in the community) and children from different age groups. We characterized ETEC isolates in terms of their colonization factors (CFs) and enterotoxins, and determined whether these factors varied with setting and age group. Diarrhoeal stool samples were obtained from children under the age of 60 months from: (1) the regional public hospital, (2) four public primary care clinics, and (3) a population-based cohort. In total, 58 ETEC-positive isolates were analysed by multiplex-PCR assays for the identification of CFs (CS1, CS2, CS3, CS4, CS5, CS6, CS7, CS8, CS12, CS13, CS14, CS15, CS17, CS18, CS19, CS20, CS21, CS22 and CFA/I), and enterotoxins [heat-labile toxin (LT) and heat-stable variants STh and STp]. The frequency of CFs and enterotoxins was compared among the three settings and for different age groups, using Fisher’s exact test or a χ2 test. At least one CF was detected among one-half of samples; CS19 was detected among all strains in which a CF was identified, either alone or in combination with another CF. Among all CFs detected, 91.7 % were identified as members of the class 5 fimbrial family. CFs were detected more commonly among samples from infants captured in the health facility setting compared with the community setting. Overall, LT was detected among 67.2 % of samples, STh was detected among 20.7 % and both enterotoxins were detected among 12.1 %. The enterotoxin STh was detected more commonly among cases in the community, whilst a combination of STh and LT was detected more commonly among cases treated in health facilities. Our results suggest that, to protect against diarrhoeal cases associated with this E. coli pathotype in León, Nicaragua, an ETEC vaccine that effectively targets the archeotype CFA/I of the class 5 fimbrial family would be the most effective in this setting.
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40

Dai, Da-nian, Yan Li, Bo Chen, et al. "Elevated expression of CST1 promotes breast cancer progression and predicts a poor prognosis." Journal of Molecular Medicine 95, no. 8 (2017): 873–86. http://dx.doi.org/10.1007/s00109-017-1537-1.

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Abstract Cystatin SN (CST1) belongs to the type 2 cystatin (CST) superfamily, which restricts the proteolytic activities of cysteine proteases. CST1 has been recently considered to be involved in the development of several human cancers. However, the prognostic significance and function of CST1 in breast cancer remains unknown. In the current study, we found that CST1 was generally upregulated in breast cancer at both mRNA and protein level. Furthermore, overall survival (OS) and disease-free survival (DFS) in the low CST1 expression subgroup were significantly superior to the high CST1 expression subgroup (OS, p < 0.001; DFS, p < 0.001), which indicated that CST1 expression level was closely correlated to the survival risk of these patients. Univariate and multivariate analyses demonstrated that CST1 expression was an independent prognostic factor, the same as ER status and nodal status. Next, CST1 overexpression promoted breast cancer cell proliferation, clonogenicity, migration, and invasion abilities. By contrast, knockdown of CST1 attenuated these malignant characteristics in breast cancer cells. Collectively, our study indicates that CST1 cannot only serve as a significant prognostic indicator but also as a potential therapeutic target for breast cancer. Key messages High CST1 expression is negatively correlated with survival of breast cancer patients. CST1 promotes cell proliferation, clone formation, and metastasis in breast cancer cells. CST1 is a novel potential prognostic biomarker and therapeutic target for breast cancer.
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41

Uemura, Satoshi, Akio Kihara, Soichiro Iwaki, Jin-ichi Inokuchi, and Yasuyuki Igarashi. "Regulation of the Transport and Protein Levels of the Inositol Phosphorylceramide Mannosyltransferases Csg1 and Csh1 by the Ca2+-binding Protein Csg2." Journal of Biological Chemistry 282, no. 12 (2007): 8613–21. http://dx.doi.org/10.1074/jbc.m606649200.

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42

liu, li. "Abstract P3-11-02: CST1 Interaction with RAB1B Modulates Tamoxifen resistance of Breast Cancer by Regulating Autophagy." Cancer Research 83, no. 5_Supplement (2023): P3–11–02—P3–11–02. http://dx.doi.org/10.1158/1538-7445.sabcs22-p3-11-02.

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Abstract Background: Breast cancer is a prominent cause of cancer-related death among women worldwide. Approximately,70% of breast cancers (BC) are estrogen and progestogen receptor-positive (HR+) at diagnosis. Adjuvant endocrine therapy is a pivotal component of treatment for this type of patient. Tamoxifen (TAM), a widely recommended drug in endocrine therapy, is confronted with a high risk of recurrence after 5 years of treatment among breast cancer patients, which shows big clinical demands. Therefore, it is urgent to find new targets for tamoxifen resistance therapy. Recently, our team found that enhanced expression of Cystain SN (CST1) was detected in tissues that had undergone tamoxifen treatment appearing to recurrence and metastasis in ER-positive breast cancer patients. However, the molecular mechanisms of modulating tamoxifen resistance remain unknown. Therefore, our team suspected that there might be a correlation between the abnormal expression of CST1 and tamoxifen resistance. To investigate whether CST1 is involved in tamoxifen resistance and its molecular mechanism, we conducted further research. It is critical to elucidate the molecular mechanisms of tamoxifen resistance and to explore a novel effective therapeutic target. Method: Enhanced expression of CST1 was confirmed by immunohistochemistry in breast cancer tissue samples and by quantitative real-time PCR in Tamoxifen-resistant cancer cell lines MCF-7R/T47DR. To further investigate the molecular function of CST1, we knockdown its expression in MCF-7R/T47DR cells by transfecting with the lentiviral particles of shCST1 and corresponding negative control (Shanghai Genechem Co., Ltd.) and overexpressed CST1 in MCF-7/T47D cells using ove-GST-CST1, ove-HA-RAB1B plasmids. The effects of CST1 on cell viability and proliferation in breast cancer cells were detected by cell counting kit-8 and colony formation assays, respectively. The interaction between CST1 and RAB1B was validated by Co-immunoprecipitation and Western blot. Autophagosomes were found using transmission electron microscopy (TEM) along with Western blotting to detect the transformation of LC3-I to LC3-II protein (i.e., the LC3-II/LC3-I ratio) and P62 protein levels. Results: We found that aberrant expression of Cystatin SN (CST1) was identified in ER-positive breast cancer (BC) cells (Figure 1) and which is crucial in contributing to Tamoxifen resistance (Figure 2). The direct promotion of autophagy by RAPA can faciliate cells to endocrine resistance. And knockdown of CST1 not only suppressed autophagy in Tamoxifen-resistant cells but also attenuated the resistance, which determined the correlation of CST1 with autophagy in BC (Figure 3). Rab1b (Ras-related protein Rab-1B), a membrane protein essential for autophagosome formation, was verified to have interaction with CST1 through Coimmunoprecipitation (CO-IP) experiments (Figure 4). Meanwhile, RAB1B expression was also reduced by CST1 knockdown in the resistant cells. The interaction between CST1 and RAB1B induces autophagy which decreases Tamoxifen’s therapeutic efficacy. Furthermore, rescue experiments suggested that CST1 knockdown–induced sensitization in the efficacy of TAM Therapy and decreased autophagy could be restored via RAB1B overexpression.Conclusions: These results indicate that CST1 interacts with RAB1B to facilitate BC resistant to TAM through regulation of autophagy and CST1 might be a potential therapeutic target to overcome endocrine therapy resistance. Figure 1. Enhanced expression of CST1 in Tamoxifen-resistance breast cancer Figure 1. Enhanced expression of CST1 in Tamoxifen-resistance breast cancer Figure 2. CST1 expression is positively correlated with autophagy in ER-positive breast cancer Figure 2. CST1 expression is positively correlated with autophagy in ER-positive breast cancer Figure 3. CST1 promotes cells resistant to tamoxifen therapy by activating auophagy Figure 3. CST1 promotes cells resistant to tamoxifen therapy by activating auophagy Figure 4. CST1 interacts with RAB1B in cell autophagy Figure 4. CST1 interacts with RAB1B in cell autophagy Citation Format: li liu. CST1 Interaction with RAB1B Modulates Tamoxifen resistance of Breast Cancer by Regulating Autophagy [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr P3-11-02.
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43

Oh, Byung Moo, Seon-Jin Lee, Hee Jun Cho, et al. "Cystatin SN inhibits auranofin-induced cell death by autophagic induction and ROS regulation via glutathione reductase activity in colorectal cancer." Cell Death & Disease 8, no. 3 (2017): e2682-e2682. http://dx.doi.org/10.1038/cddis.2017.100.

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Abstract Cystatin SN (CST1) is a specific inhibitor belonging to the cystatin superfamily that controls the proteolytic activities of cysteine proteases such as cathepsins. Our previous study showed that high CST1 expression enhances tumor metastasis and invasiveness in colorectal cancer. Recently, auranofin (AF), a gold(I)-containing thioredoxin reductase 1 (TrxR1) inhibitor, has been used clinically to treat rheumatoid arthritis. AF is a proteasome-associated deubiquitinase inhibitor and can act as an anti-tumor agent. In this study, we investigated whether CST1 expression induces autophagy and tumor cell survival. We also investigated the therapeutic effects of AF as an anti-tumor agent in colorectal cancer (CRC) cells. We found that CRC cells expressing high levels of CST1 undergo increased autophagy and exhibit chemotherapeutic resistance to AF-induced cell death, while those expressing low levels of CST1 are sensitive to AF. We also observed that knockdown of CST1 in high-CST1 CRC cells using CST1-specific small interfering RNAs attenuated autophagic activation and restored AF-induced cell mortality. Conversely, the overexpression of CST1 increased autophagy and viability in cells expressing low levels of CST1. Interestingly, high expression of CST1 attenuates AF-induced cell death by inhibiting intracellular reactive oxygen species (ROS) generation, as demonstrated by the fact that the blockage of ROS production reversed AF-induced cell death in CRC cells. In addition, upregulation of CST1 expression increased cellular glutathione reductase (GR) activity, reducing the cellular redox state and inducing autophagy in AF-treated CRC cells. These results suggest that high CST1 expression may be involved in autophagic induction and protects from AF-induced cell death by inhibition of ROS generation through the regulation of GR activity.
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44

Zhang, Lane, Limin Wang, Shu Li, Jingyi Xue, and Dali Luo. "Calsequestrin-1 Regulates Store-Operated Ca2+ Entry by Inhibiting STIM1 Aggregation." Cellular Physiology and Biochemistry 38, no. 6 (2016): 2183–93. http://dx.doi.org/10.1159/000445574.

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Background/Aims: Stromal interacting molecule-1 (STIM1) aggregation and redistribution to plasma membrane to interact with Orai1 constitute the core mechanism of store-operated Ca2+ entry (SOCE). Previous study has revealed that calsequestrin-1 (CSQ1) regulates SOCE in HEK293 cells through interacting with STIM1 and inhibiting STIM1/Orai1 interaction. Here, we further investigate how CSQ1/STIM1 interaction affects SOCE. Methods: Using confocal microscopy, STIM1 aggregation and co-localizations with CSQ1 or Orai1 upon Ca2+ store depletion by thapsigargin were measured and quantified by Imaris software in HeLa cells transfected with different CSQ1 mutants. The interactions of CSQ1/STIM1 and STIM1/Orai1, and internal Ca2+ changes were detected by co-immunoprecipitation and Fura2, respectively. Results: Wt-CSQ1 overexpression significantly reduced STIM1 clustering in the perimembrane and cytosolic regions, whereas over-expression of a C-terminal amino acid 362-396 deletion mutant (C35) did not. Consistently, a significant depression of SOCE, increased CSQ1 monomerization and CSQ1/STIM1 interaction, and a reduced STIM1/Orai1 association were observed in wt-CSQ1 but not in C35-transfected cells. Additionally, mutant lacking C-terminal AA 388-396 deletion exerted weaker potency in inhibiting STIM1 aggregation and association with Orai1 than wt-CSQ1. Conclusions: Our results demonstrate that CSQ1 monomers suppress SOCE by interacting with STIM1 and attenuating STIM1 aggregation via its C-terminal amino acid 362-396.
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45

Vodopyanov, Sergey O., Artem A. Gerasimenko, Alexey S. Vodopyanov, A. M. Gorokh, Ruslan V. Pisanov, and Vladimir D. Kruglikov. "The cold-shock gene’s protein complex of different serogroups of Vibrio cholerae." Вестник Пермского университета. Серия «Биология»=Bulletin of Perm University. Biology, no. 2 (2023): 166–71. http://dx.doi.org/10.17072/1994-9952-2023-2-166-171.

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553 whole genome sequences of Vibrio cholerae strains O1, O139 and nonO1/nonO139 serogroups were studied for the presence of cold-shock genes cspA, cspV and csh1. The cspA and cspV genes were present in almost all strains. The csh1 gene was present in 99/449 strains of the serogroup O1 and in 21/86 cultures of nonO1/nonO139 taken in the study. The absence of the csh1 gene was revealed in strains of the O139 serogroup and strains of the O1 serogroup with ctxAB and tcpA genes. The study of the nucleotide composition identified 13 different variants of the csh1 gene which cause structural differences in the cold-shock protein Csh1. The two main types of Csh1 protein were represented by the reference type (68 genomes) and the major type (35 genomes), 11 minor variants included single genomes. According to the NCBI database, mainly representatives of minor types of Csh1 protein circulate abroad. The reference type Csh1 was mainly detected in O1 serogroup strains, while 10 strains with the reference type Csh1 protein were identified before 2000, then in 2001-2022 their number reached 55 strains. It is assumed that the new cold shock gene csh1 gives vibrions a selective advantage by ensuring survival at low temperatures in reservoirs.
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46

Aharinejad, Seyedhossein, Mohamed Salama, Patrick Paulus, Karin Zins, Andreas Berger, and Christian F. Singer. "Elevated CSF1 serum concentration predicts poor overall survival in women with early breast cancer." Endocrine-Related Cancer 20, no. 6 (2013): 777–83. http://dx.doi.org/10.1530/erc-13-0198.

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Colony-stimulating factor 1 (CSF1) is a key regulator of mammary gland development, and a modulator of tissue macrophages. Expression of the CSF1 receptor geneC-FMS(CSF1R) is strongly associated with poor outcome in breast cancer and results in tumor cell invasiveness and pro-metastatic behaviorin vitro. However, CSF1's role as a predictive factor in breast cancer remains unclear. We have prospectively measured circulating CSF1 using ELISA in 572 women with early breast cancer and in 688 women with benign breast lesions, and correlated these concentrations with overall survival (OS), nodal status, and other clinical and histological parameters. Serum CSF1 concentrations were significantly elevated in patients with early breast cancer when compared with those with benign tumors (P<0.0001). Within breast cancer patients, CSF1 was higher in women with axillary lymph nodes (P=0.03). Serum CSF1 correlated with tumor size (P=0.002), age (P<0.001), and Ki67 expression (P=0.006). Log CSF1 serum concentrations were predictive of poor survival in both univariate (hazard ratio (HR): 3.77, 95% CI: 1.65–8.65,P=0.002) and multivariate analyses (HR: 3.1, 95% CI: 1.03–9.33,P=0.04). Post- but not premenopausal women with CSF1 serum concentrations >873 pg/ml experienced a significantly poorer outcome (P=0.004 log-rank test). Serum CSF1 concentrations are elevated in women with malignant breast tumors. In early breast cancer, elevated serum CSF1 is associated with nodal involvement, and in postmenopausal women also with poor OS.
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47

Lin, WeiYu, Donnie Delarosa, Judy Young, et al. "Blockade of CSF-1 and IL-34 in mouse model of inflammatory arthritis and colitis show a pathogenic role for IL-34 (P5160)." Journal of Immunology 190, no. 1_Supplement (2013): 195.9. http://dx.doi.org/10.4049/jimmunol.190.supp.195.9.

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Abstract Colony-stimulating factor1 (CSF1) and IL34 signaling through their receptor (CSF1R) promotes monocyte and macrophage (Mf) differentiation, proliferation and migration. Mf activation through CSF1/IL34 and CSF1R signaling is associated with a broad spectrum of pathologies. Therapeutic monoclonal antibodies (mAb) against CSF1 and CSF1R or specific inhibitors of CSF1R kinase activity have been tested in the animal models and some human trials. To date there are no reports on IL34 or dual CSF1 and IL34 blockade as a therapeutic strategy for targeting myeloid driven diseases. Here we describe neutralization of both CSF1 and IL34 using specific mAb in collagen induced arthritis (CIA) and DSS-induced colitis mouse models. The efficacy of the dual blockade was superior to the single blockade of CSF1 or IL34 in both models. In CIA treatment was started at day 31 post disease induction and continued for 7 weeks. Anti-CSF1 plus anti-IL34 combination therapy reduced arthritis severity comparable to anti-TNF therapy. Mechanistic studies showed reduction of Mf and monocytes in the joint of dual Ab treated group. Dual blockade of CSF1 and IL34 decreased colon histology score in colitis mice. The mice with colitis produced higher CSF1 and IL34 in serum and colon tissue compared with the controls. In conclusion, blocking CSF1 and IL34 by specific mAb could be an effective therapy for myeloid driven inflammatory disease.
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48

Zhang, Liangming, Sunxing Yu, Xiaoqing Yin, et al. "MiR-942-5p inhibits tumor migration and invasion through targeting CST1 in esophageal squamous cell carcinoma." PLOS ONE 18, no. 2 (2023): e0277006. http://dx.doi.org/10.1371/journal.pone.0277006.

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Introduction Cysteine Protease Inhibitor 1 (CST1), a cystatin superfamily protein with the effect on the inhibition of cysteine protease activity, is reported to be involved in the development of many malignancies. MiR-942-5p has been demonstrated its regulatory effects on some malignancies. However, the roles of CST1 and miR-942-5p on esophageal squamous cell carcinoma (ESCC) are still unknown up to now. Methods The expression of CST1 in ESCC tissues was analyzed by TCGA database, immunohistochemistry, and RT-qPCR, respectively. Matrigel-uncoated or-coated transwell assay was used to determine the effect of CST1 on migration and invasion of ESCC cells. Regulatory effect of miR-942-5p on CST1 was detected by dual luciferase assay. Results CST1 was ectopically highly expressed in ESCC tissues, and had the effect on promoting the migration and invasion of ESCC cells by upregulating phosphorylated levels of key effectors including MEK1/2, ERK1/2, and CREB in MEK/ERK/CREB pathway. Dual-luciferase assay results showed that miR-942-5p had a regulatory effect on targeting CST1. Conclusions CST1 plays a carcinogenic role on ESCC, and miR-942-5p can regulate the migration and invasion of ESCC cells by targeting CST1 to downregulate MEK/ERK/CREB signaling pathway, suggesting that miR-942-5p/CST1 axis might be a promising target for diagnosis and treatment of ESCC.
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49

Hu, Xiao, Shirong Li, Desislava Met Doycheva, et al. "Rh-CSF1 Attenuates Oxidative Stress and Neuronal Apoptosis via the CSF1R/PLCG2/PKA/UCP2 Signaling Pathway in a Rat Model of Neonatal HIE." Oxidative Medicine and Cellular Longevity 2020 (October 8, 2020): 1–20. http://dx.doi.org/10.1155/2020/6801587.

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Oxidative stress (OS) and neuronal apoptosis are major pathological processes after hypoxic-ischemic encephalopathy (HIE). Colony stimulating factor 1 (CSF1), binding to CSF1 receptor (CSF1R), has been shown to reduce neuronal loss after hypoxic-ischemia- (HI-) induced brain injury. In the present study, we hypothesized that CSF1 could alleviate OS-induced neuronal degeneration and apoptosis through the CSF1R/PLCG2/PKA/UCP2 signaling pathway in a rat model of HI. A total of 127 ten-day old Sprague Dawley rat pups were used. HI was induced by right common carotid artery ligation with subsequent exposure to hypoxia for 2.5 h. Exogenous recombinant human CSF1 (rh-CSF1) was administered intranasally at 1 h and 24 h after HI. The CSF1R inhibitor, BLZ945, or phospholipase C-gamma 2 (PLCG2) inhibitor, U73122, was injected intraperitoneally at 1 h before HI induction. Brain infarct volume measurement, cliff avoidance test, righting reflex test, double immunofluorescence staining, western blot assessment, 8-OHdG and MitoSOX staining, Fluoro-Jade C staining, and TUNEL staining were used. Our results indicated that the expressions of endogenous CSF1, CSF1R, p-CSF1R, p-PLCG2, p-PKA, and uncoupling protein2 (UCP2) were increased after HI. CSF1 and CSF1R were expressed in neurons and astrocytes. Rh-CSF1 treatment significantly attenuated neurological deficits, infarct volume, OS, neuronal apoptosis, and degeneration at 48 h after HI. Moreover, activation of CSF1R by rh-CSF1 significantly increased the brain tissue expressions of p-PLCG2, p-PKA, UCP2, and Bcl2/Bax ratio, but reduced the expression of cleaved caspase-3. The neuroprotective effects of rh-CSF1 were abolished by BLZ945 or U73122. These results suggested that rh-CSF1 treatment attenuated OS-induced neuronal degeneration and apoptosis after HI, at least in part, through the CSF1R/PLCG2/PKA/UCP2 signaling pathway. Rh-CSF1 may serve as therapeutic strategy against brain damage in patients with HIE.
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Wu, Jianfei, Xinmei Hu, Xinyu Peng, Xiu Zhang, Jianjun Zhang, and Peng Liu. "Role of CST1 in Promoting Gastric Cancer Metastasis and Analysis of Its Mechanism." Proceedings of Anticancer Research 7, no. 3 (2023): 58–63. http://dx.doi.org/10.26689/par.v7i3.4861.

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Objective: To elucidate the role and mechanism of cysteine protease inhibitor SN (CST1) in promoting the metastasis of gastric cancer. Methods: (1) Firstly, 6 pairs of cancer and paracancer tissue samples from gastric cancer patients without distant metastasis and 5 pairs of cancer and paracancer tissue samples from gastric cancer patients with peritoneal metastasis were collected for transcriptome sequencing. Statistical analysis was performed on the sequencing results to identify significantly upregulated differential genes. (2) Another 75 pairs of cancer and paracancer tissue samples were collected from gastric cancer patients, and the protein and total RNA of gastric cancer tissue samples were extracted. Western blot and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were used to detect the expression of CST1 protein and messenger RNA (mRNA) in gastric cancer and adjacent tissues. (3) The total protein and total RNA of AGS, BGC823, HGC-27, MGC803, MKN45, SGC7901, and SNU-1 gastric cancer cells and normal gastric mucosal epithelial cells GES-1 were extracted. Western blot and qRT-PCR were used to detect CST1 protein and mRNA expression. Results: (1) The significantly upregulated differential gene CST1 was screened, and the expression of CST1 in gastric cancer tissues was significantly higher than that in adjacent tissues. (2) Compared with normal gastric mucosal epithelial cells GES-1, the expression of CST1 in gastric cancer cell lines was upregulated, and the expression of CST1 in HGC-27 and SNU-1 was relatively low, while the expression of CST1 in AGS and MKN45 was relatively high. At the same time, a stable cell line of HGC-27 overexpressing CST1 and MKN45 knocking down CST1 was successfully constructed. (3) Overexpression or knockdown of CST1 did not significantly change the proliferation ability of gastric cancer cells, but can promote the migration and invasion of gastric cancer cells. (4) CST1 may promote the metastasis of gastric cancer cells by activating the epithelial–mesenchymal transition (EMT) signaling pathway. Conclusion: CST1 gene promotes the migration of gastric cancer cells, and we found through animal experiments that CST1 can affect the metastasis and invasion function of gastric cancer and is negatively correlated with the level of E-cadherin.
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