Anti-MNAT1 Monoclonal Antibody (DCABH- 200971) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use

Anti-MNAT1 monoclonal antibody (DCABH- 200971) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Antigen Description The protein encoded by this gene, along with cyclin H and CDK7, forms the CDK-activating kinase (CAK) enzymatic complex. This complex activates several cyclin-associated kinases and can also associate with TFIIH to activate transcription by RNA polymerase II. Two transcript variants encoding different isoforms have been found for this gene. Immunogen A synthetic peptide of human MNAT1 is used for rabbit immunization. Isotype IgG Source/Host Rabbit Species Reactivity Mouse, Rat, Human Purification Protein A Conjugate Unconjugated Applications FC, ICC/IF, WB Size 100 μl Buffer Preservative: 0.01% Sodium azide Constituents: 9% PBS, 40% Glycerol, 0.05% BSA, 50% Tissue culture supernatant, Preservative None Storage Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing. GENE INFORMATION Gene Name MNAT1 MNAT CDK-activating kinase assembly factor 1 [ Homo sapiens (human) ] Official Symbol MNAT1 Synonyms MNAT1; MNAT CDK-activating kinase assembly factor 1; MAT1; TFB3; CAP35; RNF66; CDK- activating kinase assembly factor MAT1; RING finger protein 66; RING finger protein MAT1; CDK7/cyclin-H assembly factor; cyclin G1 interacting protein; cyclin-G1-interacting protein; 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved menage a trois 1 (CAK assembly factor); menage a trois homolog 1, cyclin H assembly factor; Entrez Gene ID 4331 Protein Refseq NP_001171434 UniProt ID A0A024R669 Chromosome Location 14q23 Pathway Basal transcription factors; Cell Cycle; Cell Cycle, Mitotic; Cyclin A/B1 associated events during G2/M transition; Cyclin A:Cdk2-associated events at S phase entry; Cyclin D associated events in G1; Cyclin E associated events during G1/S transition; DNA Repair; Disease; Dual incision reaction in GG-NER; Dual incision reaction in TC-NER; Function contributes_to DNA-dependent ATPase activity; contributes_to RNA polymerase II carboxy- terminal domain kinase activity; protein N-terminus binding; protein binding; zinc ion binding; 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 2 © Creative Diagnostics All Rights Reserved.

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A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
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Supplementary Materials
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Zhou et al. Journal of Experimental & Clinical Cancer Research (2018) 37:284 https://doi.org/10.1186/s13046-018-0956-3 RESEARCH Open Access MNAT1 is overexpressed in colorectal cancer and mediates p53 ubiquitin- degradation to promote colorectal cancer malignance Shan Zhou1,2†, Jinping Lu2†, Yuejin Li1†, Chan Chen2, Yongqiang Cai2, Gongjun Tan2, Zhengke Peng2, Zhenlin Zhang2, Zigang Dong3, Tiebang Kang4 and Faqing Tang1* Abstract Background: MNAT1 (menage a trois 1, MAT1), a cyclin-dependent kinase-activating kinase (CAK) complex, high expresses in various cancers and is involved in cancer pathogenesis. However, mechanisms underlying its regulation in carcinogenesis are unclear. Methods: The tissue microarray of colorectal cancer (CRC) was used to evaluate MNAT1 expressions in CRC tissues using immunohistochemistry, CRC cell lines were also detected MNAT1 expression using Western-blotting. MNAT1 and shMNAT1 vectors were constructed, and transfected into CRC cells. Cell growths of the transfected cells were observed using MTT and colony formation. The affects of MNAT1 on p53 expression were analyzed using Western- blotting and Real-time PCR. Immunoprecipitation assay was used to analyze the interaction p53 and MNAT1, and Western-blotting was used to test the effects of MNAT1 on p53 downstream molecules. The apoptosis of CRC cells with MNAT1 or shMNAT1 were analyzed using flow cytometry. BABL/c athymic nude mice were used to observe the effect of MNAT1 on CRC cell growth in vivo. Results: MNAT1 was found to be overexpressed in CRC tissues and cells, and MNAT1 expressions in CRC tissue samples were associated with CRC carcinogenesis and poor patient outcomes. MNAT1-knockin increased CRC cell growth and colony formation, and MNAT1-knockdown dramatically decreased cell motility and invasion.
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