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Academic literature on the topic 'MTCH2'

Author: Grafiati

Published: 6 September 2023

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Journal articles on the topic "MTCH2"

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Manjunath, Lekha E., Anumeha Singh, Sarthak Sahoo, Ashutosh Mishra, Jinsha Padmarajan, Chaithanya G. Basavaraju, and Sandeep M. Eswarappa. "Stop codon read-through of mammalian MTCH2 leading to an unstable isoform regulates mitochondrial membrane potential." Journal of Biological Chemistry 295, no. 50 (October 7, 2020): 17009–26. http://dx.doi.org/10.1074/jbc.ra120.014253.

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Stop codon read-through (SCR) is a process of continuation of translation beyond a stop codon. This phenomenon, which occurs only in certain mRNAs under specific conditions, leads to a longer isoform with properties different from that of the canonical isoform. MTCH2, which encodes a mitochondrial protein that regulates mitochondrial metabolism, was selected as a potential read-through candidate based on evolutionary conservation observed in the proximal region of its 3′ UTR. Here, we demonstrate translational read-through across two evolutionarily conserved, in-frame stop codons of MTCH2 using luminescence- and fluorescence-based assays, and by analyzing ribosome-profiling and mass spectrometry (MS) data. This phenomenon generates two isoforms, MTCH2x and MTCH2xx (single- and double-SCR products, respectively), in addition to the canonical isoform MTCH2, from the same mRNA. Our experiments revealed that a cis-acting 12-nucleotide sequence in the proximal 3′ UTR of MTCH2 is the necessary signal for SCR. Functional characterization showed that MTCH2 and MTCH2x were localized to mitochondria with a long t1/2 (>36 h). However, MTCH2xx was found predominantly in the cytoplasm. This mislocalization and its unique C terminus led to increased degradation, as shown by greatly reduced t1/2 (<1 h). MTCH2 read-through–deficient cells, generated using CRISPR-Cas9, showed increased MTCH2 expression and, consistent with this, decreased mitochondrial membrane potential. Thus, double-SCR of MTCH2 regulates its own expression levels contributing toward the maintenance of normal mitochondrial membrane potential.

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Guna, Alina, Taylor A. Stevens, Alison J. Inglis, Joseph M. Replogle, Theodore K. Esantsi, Gayathri Muthukumar, Kelly C. L. Shaffer, et al. "MTCH2 is a mitochondrial outer membrane protein insertase." Science 378, no. 6617 (October 21, 2022): 317–22. http://dx.doi.org/10.1126/science.add1856.

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In the mitochondrial outer membrane, α-helical transmembrane proteins play critical roles in cytoplasmic-mitochondrial communication. Using genome-wide CRISPR screens, we identified mitochondrial carrier homolog 2 (MTCH2), and its paralog MTCH1, and showed that it is required for insertion of biophysically diverse tail-anchored (TA), signal-anchored, and multipass proteins, but not outer membrane β-barrel proteins. Purified MTCH2 was sufficient to mediate insertion into reconstituted proteoliposomes. Functional and mutational studies suggested that MTCH2 has evolved from a solute carrier transporter. MTCH2 uses membrane-embedded hydrophilic residues to function as a gatekeeper for the outer membrane, controlling mislocalization of TAs into the endoplasmic reticulum and modulating the sensitivity of leukemia cells to apoptosis. Our identification of MTCH2 as an insertase provides a mechanistic explanation for the diverse phenotypes and disease states associated with MTCH2 dysfunction.

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Khan, Dilshad H., Michael Mullokandov, Yan Wu, Marcela Gronda, Rose Hurren, Xiaoming Wang, Neil MacLean, Rob C. Laister, Atan Gross, and Aaron D. Schimmer. "The Mitochondrial Carrier Homolog 2 (MTCH2) Regulates the Differentiation of AML Cells By Influencing the Localization of Pyruvate Dehydrogenase Complex and H3 and H4 Histone Acetylation." Blood 128, no. 22 (December 2, 2016): 1562. http://dx.doi.org/10.1182/blood.v128.22.1562.1562.

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Abstract Mitochondrial carrier homolog 2 (MTCH2) is a mitochondrial outer membrane protein that functions as a receptor-like protein for pro-apoptotic BID. In addition to its role in apoptosis, recent findings show that MTCH2 also regulates cellular metabolism. In murine hematopoietic cells, loss of MTCH2 increases oxidative phosphorylation and reduces the number of hematopoietic stem cells. Here, we sought to understand the role of MTCH2 in leukemogenesis and knocked down MTCH2 in leukemia cell lines using multiple independent shRNAs. Knockdown of MTCH2 reduced growth and viability of AML cells: OCI-AML2 (>90%), TEX (>80%), U937 (>65%), and HL60 (>75%). MTCH2 knockdown also decreased the clonogenic growth of OCI-AML2 (>60%), TEX (>70%), and U937 (>40%) cells compared to controls. However, MTCH2 knockdown did not induce cell death as indicated by annexin V/PI staining. In addition, knockdown of MTCH2 in TEX cells reduced engraftment into the marrow of non-obese diabetic/severe combined immunodeficiency-growth factor (NOD/SCID-GF) mice (control 17±4%, n=10) vs. sh-MTCH2 (4±0.86%, n=10). In mouse models, knockout of MTCH2 decreased the leukomogenic potential of murine hematopoietic stem cells transformed with the MLL-AF9 oncogene and increased the survival of these mice. To understand the mechanism by which MTCH2 knockdown decreased cell growth, we used genome wide transcriptome analysis with RNA-seq and observed an up regulation of genes involved in cellular differentiation. Consistent with increased MTCH2 knockdown promoting differentiation, OCI-AML2 cells with MTCH2 knockdown displayed increased non-specific esterase staining. Increased differentiation (Lin+ve cells) was also observed in MLL-AF9 with MTCH2 knockout. Knockdown of MTCH2 in TEX and OCI-AML2 cells increased levels of H3 and H4 histone acetylation as demonstrated by immunoblotting. Of note, differentiation and increased H3 and H4 acetylation was not observed after inhibiting other mitochondrial processes, such as mitochondrial protein synthesis or mitochondrial DNA replication. Although MTCH2 is a receptor for BID, the increased H3 and H4 acetylation appeared independent of BID as small molecule BID inhibitors did not alter H3 and H4 acetylation. MTCH2 regulates cell metabolism. Therefore, we measured changes in intracellular metabolites in AML cells after MTCH2 knockdown. In AML cells, MTCH2 knockdown increased levels of lactate (2 fold), but did not change the basal rate of oxygen consumption or the activity of mitochondrial respiratory chain complexes. Loss of mitochondrial pyruvate dehydrogenase complex increases lactate levels and a recent study reported that the translocation of pyruvate dehydrogenase complex from the mitochondria to the nucleus under conditions of mitochondrial stress, increases H3 and H4 histone acetylation (Cell. 2014; 158(1):84-97). Therefore, we measured changes in the localization of pyruvate dehydrogenase complex after MTCH2 knockdown. Knockdown of MTCH2 decreased mitochondrial and increased nuclear dehydrogenase complex in OCI-AML2 and TEX cells. Thus, in summary, MTCH2 regulates the differentiation of AML cells and controls the localization of pyruvate dehydrogenase complex and histone acetylation. These results also suggest a mechanism by which loss of MTCH2 leads to reductions of normal hematopoietic stem cells. Disclosures Schimmer: Novartis: Honoraria.

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Kulyté, Agné, Mikael Rydén, Niklas Mejhert, Elisabeth Dungner, Eva Sjölin, Peter Arner, and Ingrid Dahlman. "MTCH2 in Human White Adipose Tissue and Obesity." Journal of Clinical Endocrinology & Metabolism 96, no. 10 (October 1, 2011): E1661—E1665. http://dx.doi.org/10.1210/jc.2010-3050.

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Abstract Context: Genome-wide association studies have identified single-nucleotide polymorphisms in approximately 40 loci associated with obesity-related traits. How these loci regulate obesity is largely unknown. One obesity-associated single-nucleotide polymorphism is close to the MTCH2 gene (mitochondrial carrier homolog 2). Objective: The objective of the study was to assess the expression of genes in obesity-associated loci in abdominal sc white adipose tissue (scWAT) in relation to obesity. A more comprehensive expression study was performed on MTCH2. Design: mRNA levels of 66 genes from 40 loci were determined by microarray in scWAT from lean and obese women (n = 30). MTCH2 mRNA was measured by quantitative RT-PCR in lean and obese before and after weight loss in intact adipose pieces and isolated adipocytes, paired samples of scWAT and omental WAT, and primary adipocyte cultures (n = 191 subjects in total). MTCH2 genotypes were compared with mRNA expression in 96 women. MTCH2 protein was examined in scWAT of 38 individuals. Results: Adipose expression of eight genes was significantly associated with obesity; of these, MTCH2 displayed the highest absolute signal. MTCH2 mRNA and protein expression was significantly increased in obese women but was not affected by weight loss. MTCH2 was enriched in isolated fat cells and increased during adipocyte differentiation. There was no cis influence of MTCH2 genotypes on mRNA levels. Conclusion: MTCH2 is highly expressed in human WAT and adipocytes with increased levels in obese women. These results suggest that MTCH2 may play a role in cellular processes underlying obesity.

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Dudko, H. V., V. A. Urban, and V. G. Veresov. "Molecular mechanisms of high-affinity interaction of the protein tBid with the mitochondrial complex МТСН2-МОАР-1." Doklady of the National Academy of Sciences of Belarus 64, no. 2 (May 17, 2020): 193–98. http://dx.doi.org/10.29235/1561-8323-2020-64-2-193-198.

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Mitochondrial carrier homolog 2 (MTCH2) is a protein that plays an important role in the execution of apoptosis being a receptor for tBid in the outer membrane of mitochondria. Previously, it has been shown that the binding of the modulator of apoptosis-1 (MOAP-1) protein to MTCH2 is required for the efficient MTCH2-mediated recruitment of tBid to mitochondria and, in contrast, tBid is required for the MOAP-1 recruitment to mitochondria, but the structure understanding of these phenomena is absent. In this study, we have provided structural insights into the mechanisms of regulation of the MTCH2 receptor function for tBid by MOAP-1.

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Grinberg, Michal, Michal Schwarz, Yehudit Zaltsman, Tzipi Eini, Hagit Niv, Shmuel Pietrokovski, and Atan Gross. "Mitochondrial Carrier Homolog 2 Is a Target of tBID in Cells Signaled To Die by Tumor Necrosis Factor Alpha." Molecular and Cellular Biology 25, no. 11 (June 1, 2005): 4579–90. http://dx.doi.org/10.1128/mcb.25.11.4579-4590.2005.

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ABSTRACT BID, a proapoptotic BCL-2 family member, plays an essential role in the tumor necrosis factor alpha (TNF-α)/Fas death receptor pathway in vivo. Activation of the TNF-R1 receptor results in the cleavage of BID into truncated BID (tBID), which translocates to the mitochondria and induces the activation of BAX or BAK. In TNF-α-activated FL5.12 cells, tBID becomes part of a 45-kDa cross-linkable mitochondrial complex. Here we describe the biochemical purification of this complex and the identification of mitochondrial carrier homolog 2 (Mtch2) as part of this complex. Mtch2 is a conserved protein that is similar to members of the mitochondrial carrier protein family. Our studies with mouse liver mitochondria indicate that Mtch2 is an integral membrane protein exposed on the surface of mitochondria. Using blue-native gel electrophoresis we revealed that in viable FL5.12 cells Mtch2 resides in a protein complex of ca. 185 kDa and that the addition of TNF-α to these cells leads to the recruitment of tBID and BAX to this complex. Importantly, this recruitment was partially inhibited in FL5.12 cells stably expressing BCL-XL. These results implicate Mtch2 as a mitochondrial target of tBID and raise the possibility that the Mtch2-resident complex participates in the mitochondrial apoptotic program.

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Khan, Dilshad H., Michael Mullokandov, Yan Wu, Veronique Voisin, Marcela Gronda, Rose Hurren, Xiaoming Wang, et al. "Mitochondrial carrier homolog 2 is necessary for AML survival." Blood 136, no. 1 (July 2, 2020): 81–92. http://dx.doi.org/10.1182/blood.2019000106.

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Abstract Through a clustered regularly insterspaced short palindromic repeats (CRISPR) screen to identify mitochondrial genes necessary for the growth of acute myeloid leukemia (AML) cells, we identified the mitochondrial outer membrane protein mitochondrial carrier homolog 2 (MTCH2). In AML, knockdown of MTCH2 decreased growth, reduced engraftment potential of stem cells, and induced differentiation. Inhibiting MTCH2 in AML cells increased nuclear pyruvate and pyruvate dehydrogenase (PDH), which induced histone acetylation and subsequently promoted the differentiation of AML cells. Thus, we have defined a new mechanism by which mitochondria and metabolism regulate AML stem cells and gene expression.

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8

Cogliati, Sara, and Luca Scorrano. "A BID on mitochondria with MTCH2." Cell Research 20, no. 8 (July 13, 2010): 863–65. http://dx.doi.org/10.1038/cr.2010.100.

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Gross, Atan. "MTCH2: A new player in mitochondria biology." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1857 (August 2016): e14. http://dx.doi.org/10.1016/j.bbabio.2016.04.382.

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Moyer, Sydney M., Nina Ilic, Sydney Gang, Taylor E. Arnoff, and William C. Hahn. "Abstract 2361: MYC-driven breast cancer tumorigenesis is dependent on normal mitochondrial function." Cancer Research 82, no. 12_Supplement (June 15, 2022): 2361. http://dx.doi.org/10.1158/1538-7445.am2022-2361.

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Abstract While the transcription factor MYC is amplified in all breast cancer subtypes, nearly 60% of patients with triple-negative tumors have elevated MYC copy number and expression. Patients with triple-negative breast cancer (TNBC) typically have increased metastasis, decreased response to therapies, and poor outcomes, highlighting MYC’s causal association with disease aggressiveness and low survival rates. Unfortunately, MYC is not considered directly pharmacologically tractable. Therefore, we sought to identify collateral “genetic dependencies,” downstream of oncogenic MYC. Using comparative genome-scale CRISPR/Cas9 screening in isogenic human mammary epithelial cells (HMECs), we have identified two mitochondrial membrane transporter genes, TIMM17A and MTCH2, specifically required for MYC-dependent proliferation and survival. Since MYC is suspected to drive metabolic reprogramming in cancers, we assessed how MYC affected mitochondrial protein content by quantitative mass spectrometry. This revealed an increase in N-acetylaspartate (NAA) in HMECs with MYC amplification compared to other genetic backgrounds. Interestingly, increased NAA levels are dependent on TIMM17A and MTCH2 presence. Loss of either of these genes results in cell death coupled with decreased NAA. NAA supplementation in the media of MYC-HMECs following loss of TIMM17A or MTCH2 can rescue the cell death. Importantly, NAA supplementation in cells with guides targeting GFP (negative control) or general essential gene RPL11 did not show increased cell growth/viability - showing that the NAA supplementation is specifically compensating for loss of mitochondrial transport function in MYC-HMECs. Based on these data, it appears that MYC-amplified TNBCs are uniquely dependent on TIMM17A and MTCH2 mitochondrial transporter function because they drive metabolic reprogramming resulting in addiction to N-acetylaspartate production. To conclude these studies, we are evaluating the dependence on mitochondrial transport and NAA synthesis in MYC-amplified TNBCs by assessing the function of TIMM17A and MTCH2 as MYC-specific genetic dependencies in patient derived xenografts of TNBC and determining if TNBCs are addicted to increased NAA synthesis by overexpressing aspartoacylase to breakdown NAA. Successful completion of this work will provide novel drug targets required for survival of aggressive MYC-amplified breast cancers. Citation Format: Sydney M. Moyer, Nina Ilic, Sydney Gang, Taylor E. Arnoff, William C. Hahn. MYC-driven breast cancer tumorigenesis is dependent on normal mitochondrial function [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2361.

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Books on the topic "MTCH2"

1

Mayfair. MIX/MTCH HOME DECORATION. Hamlyn, 1995.

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Dunn, Phoebe. BIG & LITTLE: MTCHM OPP (Matchem Board Books). Random House Books for Young Readers, 1988.

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Dunn, Phoebe. HOW MANY? MTCHM COUNTG (Matchem Board Books). Random House Books for Young Readers, 1988.

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Zaragoza, Txema Bañón, and Txema Bañón. Las 12 Sales Bioquímicas Constitucionales Del Dr. Wilhem Schüssler. Los 38 Remedios Florales Del Dr. Edward Bach, y Los 8 Temperamentos Asociados de la MTCH. Independently Published, 2020.

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Book chapters on the topic "MTCH2"

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Gupta, Alpana, and Athar Hussain. "Perspectives on Climate Smart Agriculture." In Practice, Progress, and Proficiency in Sustainability, 225–48. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-7998-9557-2.ch012.

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Agriculture is one of India's most significant industries, serving half of the nation. Climate is a big factor for agricultural production. Agriculture is primarily rain-fed and subjected by small-scale farmers. Rain-fed crops are 48% of the overall area under food crops and 68% on non-food crops. The complete worldwide agricultural production in India accounts for 7.39%. India's total emissions from all GHGs in 2014, according to the World Resource Institutes, total about 3,200 MTCO2 eq out of 48,892 MTCO2s eq worldwide in 2014. Agriculture is ascribed 626.86 2 MTCO2 eq of the Indian greenhouse gas emissions averaged in 2014 of 3,200 MTCO2 eq. This chapter reviews the concept of sustainable agriculture, establishes the link between climate change and agriculture, the origination of climate-smart agriculture, and relevant practical approaches, case studies, and geospatial assessment methods responding to climate-smart agriculture.

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Conference papers on the topic "MTCH2"

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Carvalho, Marco M., Thomas C. Eskridge, Larry Bunch, Jeffrey M. Bradshaw, Adam Dalton, Paul Feltovich, James Lott, and Daniel Kidwell. "A human-agent teamwork command and control framework for moving target defense (MTC2)." In the Eighth Annual Cyber Security and Information Intelligence Research Workshop. New York, New York, USA: ACM Press, 2013. http://dx.doi.org/10.1145/2459976.2460019.

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Carvalho, Marco, Thomas C. Eskridge, Larry Bunch, Adam Dalton, Robert Hoffman, Jeffrey M. Bradshaw, Paul J. Feltovich, Daniel Kidwell, and Teresa Shanklin. "MTC2: A command and control framework for moving target defense and cyber resilience." In 2013 6th International Symposium on Resilient Control Systems (ISRCS). IEEE, 2013. http://dx.doi.org/10.1109/isrcs.2013.6623772.

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Bousseksou, Adel, Yannick Chassagneux, Raffaele Colombelli, Arthur Babuty, Yannick De Wilde, Gille Patriarche, G. Beaudoin, and Isabelle Sagnes. "Surface-Plasmons on Structured Metallic Surfaces: Theoretical Analysis, Applications to Mid-Infrared Quantum Cascade Lasers and a-SNOM Survey." In Plasmonics and Metamaterials. Washington, D.C.: OSA, 2008. http://dx.doi.org/10.1364/meta_plas.2008.mthc2.

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Ott, A. W., A. C. Dillon, H. K. Eaton, S. M. George, and J. D. Way. "Atomic Layer Controlled Deposition Of Al2O3 Films Employing Trimethylaluminum (TMA) And H2O Vapor." In Microphysics of Surfaces: Nanoscale Processing. Washington, D.C.: Optica Publishing Group, 1995. http://dx.doi.org/10.1364/msnp.1995.mthc2.

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The development of atomic layer controlled deposition processes has been a focus of recent research(1). The controlled growth of Al2O3 thin films has several important technological applications. For example, Al2O3 deposition on silicon surfaces is useful for the low temperature formation of high dielectric insulators.

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Reports on the topic "MTCH2"

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Alshehri, Thamir, Jan Frederik Braun, Anwar Gasim, and Mari Luomi. What Drove Saudi Arabia’s 2020 Fall in CO2 Emissions? King Abdullah Petroleum Studies and Research Center, December 2021. http://dx.doi.org/10.30573/ks--2021-ii10.

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In June 2021, the energy data provider Enerdata released its initial estimates for Saudi Arabia’s 2020 carbon dioxide (CO2) emissions. The data indicate that the Kingdom’s CO2 emissions from fuel combustion decreased by 3.3%, from 508.3 million tonnes of CO2 (MtCO2) in 2019 to 491.8 megatonnes of CO2 (MtCO2) in 2020.

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Dooley, James J. Visualizing the Surface Infrastructure Used to Move 2 MtCO2/year from the Dakota Gasification Company to the Weyburn CO2 Enhanced Oil Recovery Project: Version of July 1, 2009. Office of Scientific and Technical Information (OSTI), July 2009. http://dx.doi.org/10.2172/989054.

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Petit, Vincent. Road to a rapid transition to sustainable energy security in Europe. Schneider Electric Sustainability Research Institute, October 2022. http://dx.doi.org/10.58284/se.sri.bcap9655.

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Decarbonization and energy security in Europe are two faces of the same coin. They are both related to the large dependency of the European Union economy on fossil fuels, which today represent around 70% of the total supply of energy. The bulk of these energy resources are imported, with Russia being the largest supplier, accounting for 40% of natural gas and 27% of oil imports. However, fossil fuels are also the primary root cause of greenhouse gas emissions, and the European Union is committed to reduce those by 55% by 2030 (versus 1990). This report is based on the landmark research from the Joint Research Center of the European Commission, the “Integrated Database of the European Energy Sector”, which for the first time mapped actual energy uses for each country within the European Union, across 17 sectors of activity, with data granularity at the level of each process step (or end-use) of each of these sectors. Our approach here has been to systematically review these process steps (or end-uses) and qualify the extent to which they could be electrified, effectively removing the demand for fossil fuels as a result. We have focused only on those process steps where technology was already widely available and for which we evaluated the switch to be relatively easy (or attractive). In other words, we estimated the impact of rapid electrification of “easy to abate” activities. The conclusion of this evaluation is that the share of electricity demand in the final energy mix could jump from around 20% today to 50%, which would drive a reduction in emissions at end-use of around 1,300 MtCO2 /y, as well as a drop in natural gas and oil supply of around 50%. As a result of such transformation, electricity demand would nearly double, with the bulk of that growth materializing in the building sector. Short-term, the challenge of addressing climate targets while providing for energy security is thus intimately connected to buildings. While such transition would certainly require major infrastructure upgrades, which may prove a roadblock to rapid deployment, we find that the combination of energy efficiency measures (notably digital) and distributed generation penetration (rooftop solar) could significantly tame the issue, and hence help accelerate the move away from fossil fuels, with energy spend savings as high as 80% across some building types; a major driver of change. Beyond this, further potential exists for electrification. Other measures on the demand-side will include deeper renovations of the industrial stock (notably in the automotive, machinery, paper, and petrochemical industries for which our current assessment may be underestimated) and further electrification of mobility (trucks). The transition of the power system away from coal (and ultimately natural gas) will then also play a key role, followed ultimately by feedstocks substitution in industry. Some of these transitions are already on the way and will likely bring further improvements. The key message, however, is that a significant opportunity revolves around buildings to both quickly decarbonize and reduce energy dependencies in Europe. Rapid transformation of the energy system may be more feasible than we think. We notably estimate that, by 2030, an ambitious and focused effort could help displace 15% to 25% of natural gas and oil supply and reduce emissions by around 500 MtCO2 /y (note that these savings would come on top of additional measures regarding energy efficiency and flexibility, which are not the object of this study). For this to happen, approximately 100 million buildings will need renovating, and a similar number of electric vehicles would need to hit the road.

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