Bs-6797R-Cy5.5 [Conjugated Primary Antibody]

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bs-6797R-Cy5.5 [Conjugated Primary Antibody] Rabbit Anti-CRR9 Polyclonal Antibody, Cy5.5 Conjugated www.biossusa.com [email protected] 800.501.7654 [DOMESTIC] +1.781.569.5821 [INTERNATIONAL] D A T A S H E E T Host: Rabbit Conjugation: Cy5.5 Target Protein: CRR9 Excitation/ 675nm/694nm Emission: Clonality: Polyclonal Isotype: IgG Size: 100ul Entrez Gene: 81037 Concentration: 1ug/ul Swiss Prot: Applications: IF(IHC-P)(1:50-200) Source: KLH conjugated synthetic peptide derived from human CLPTM1L/CRR9 Cross Reactive Human Species: Mouse Purification: Purified by Protein A. Rat Storage: Aqueous buffered solution containing 100ug/ml BSA, 50% glycerol and 0.09% sodium azide. Store at 4°C for 12 months. Caution: For research use only. Not for human or animal therapeutic or diagnostic use. Background: Clefts of the oral-facial region usually occur in early fetal development and can affect the lip, the soft palate and the hard palate. Cleft lip (with or without cleft palate) is a genetically complex birth defect that occurs in approximately one in every 750-1,000 live births. This is one of the most common birth defects and is multifactorial, with both genetic and environmental causes. Cleft lip- and palate-associated transmembrane protein 1 (CLPTM1) belongs to a family of cleft lip and palate transmembrane proteins. This family also contains cisplatin resistance-related protein (CRR9), which is involved in CDDP-induced apoptosis. CLPTM1L (cleft lip and palate transmembrane protein 1-like protein), also known as CRR9p (cisplatin resistance-related protein 9) is a 538 amino acid multi-pass membrane protein that belongs to the CLPTM1 family and, when overexpressed, enhances cisplatin-mediated apoptosis. CLPTM1L exists as two alternatively spliced isoforms encoded by a gene that maps to human chromosome 5p15.33. .

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Dong et al. Genome Medicine (2021) 13:110 https://doi.org/10.1186/s13073-021-00927-6 RESEARCH Open Access A global overview of genetically interpretable multimorbidities among common diseases in the UK Biobank Guiying Dong1,2, Jianfeng Feng1,2,3, Fengzhu Sun4, Jingqi Chen1,2,3* and Xing-Ming Zhao1,2,3* Abstract Background: Multimorbidities greatly increase the global health burdens, but the landscapes of their genetic risks have not been systematically investigated. Methods: We used the hospital inpatient data of 385,335 patients in the UK Biobank to investigate the multimorbid relations among 439 common diseases. Post-GWAS analyses were performed to identify multimorbidity shared genetic risks at the genomic loci, network, as well as overall genetic architecture levels. We conducted network decomposition for the networks of genetically interpretable multimorbidities to detect the hub diseases and the involved molecules and functions in each module. Results: In total, 11,285 multimorbidities among 439 common diseases were identified, and 46% of them were genetically interpretable at the loci, network, or overall genetic architecture levels. Multimorbidities affecting the same and different physiological systems displayed different patterns of the shared genetic components, with the former more likely to share loci-level genetic components while the latter more likely to share network-level genetic components. Moreover, both the loci- and network-level genetic components shared by multimorbidities converged on cell immunity, protein metabolism, and gene silencing. Furthermore, we found that the genetically interpretable multimorbidities tend to form network modules, mediated by hub diseases and featuring physiological categories. Finally, we showcased how hub diseases mediating the multimorbidity modules could help provide useful insights for the genetic contributors of multimorbidities.
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216141 2 En Bookbackmatter 461..490
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Platform Abstracts
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