Anti-MYCL1 polyclonal antibody (CABT-BL5216)

Rabbit Anti-Human MYCL1 (aa 105-154) polyclonal antibody for IHC-P, WB


Host Species
Antibody Isotype
Species Reactivity
Mouse, Human
A region within synthetic peptide: LERAVSDRLA PGAPRGNPPK ASAAPDCTPS LEAGNPAPAA PCPLGEPKTQ, corresponding to internal sequence amino acids 105-154 of Human l-Myc.


Application Notes
IHC-P: 4-8μg/ml
WB: 2.5μg/ml
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.


Alternative Names
MYCL1; v-myc myelocytomatosis viral oncogene homolog 1, lung carcinoma derived (avian); MYCL, v myc avian myelocytomatosis viral oncogene homolog 1, lung carcinoma derived; protein L-Myc-1; bHLHe38; l myc protein
Entrez Gene ID
UniProt ID


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Allelotype and loss of heterozygosity around the L-myc gene locus in primary lung cancers


Authors: Mendoza, C; Sato, H; Hiyama, K; Ishioka, S; Isobe, T; Maeda, H; Hiyama, E; Inai, K; Yamakido, M

L-myc S-allele was reported to be associated with metastasis of lung cancer, indicating the existence of a putative tumor suppressor gene around the L-myc locus, in linkage disequilibrium. The relationship between the S-allele and inactivation of some tumor suppressor gene should be indicated by allelic loss. Therefore, we examined the association between the L-myc S-allele and loss of heterozygosity at 11 loci around the L-myc locus (1p34.3) in primary lesions or other biological characteristics in lung cancer. No associations between the S-allele and allelic loss around the L-myc locus or other characteristics were Found. According to the deletion map, three shortest regions of overlap between D1S230 and D1S76 were identified. While loss of heterozygosity at SRO1, between D1S2797 and MYCL1, showed no relationship with the pathological stage, it was more frequently observed in squamous cell carcinoma than adenocarcinoma (P = 0.019), and associated with high telomerase activity (P = 0.046), an indicator of cellular immortality. in conclusion, we found three shortest regions of overlap (SROs) from D1S2797 to pter, and a tumor suppressor gene, which might be associated with suppression of lung cancer development but not with L-myc S-allele, may exist in SRO1. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.

An early lesion in hepatic carcinogenesis: Loss of heterozygosity in human cirrhotic livers and dysplastic nodules at the 1p36-p34 region


Authors: Sun, M; Eshleman, JR; Ferrell, LD; Jacobs, G; Sudilovsky, EC; Tuthill, R; Hussein, MR; Sudilovsky, O

Loss of heterozygosity (LOH) of chromosome I has been suggested, by karyotyping, to be an initial episode in human hepatocarcinogenesis. However, this alteration has not yet been investigated in cirrhotic nodules (CNs) or dysplastic nodules (DNs). In an initial study from explanted or resected cirrhotic livers, LOH in 1p36-p32 was examined in 31 hepatocellular carcinomas (HCCs), 25 low-grade dysplastic nodules (LGDNs), and 24 high-grade dysplastic nodules (HGDNs). In HCCs, LOH was detected most frequently at loci D1S2843 (1p36.1) (28.6%), D1S513 (1p34.3) (29.2%), and MYCL1 (1p34.1) (28.6%). In HGDN and LGDN, LOH incidences at D1S513 were 11.1% and 13.6%, respectively. To further refine those results and to determine sequential relationships among CN, DN, and HCC, LOH was next studied in an additional 53 HCCs, 56 HGDNs, 30 LGDNs, and 215 CNs from 11 explanted human cirrhotic livers, including 30 "nodule-in-nodule" lesions. Seven markers between D1S2843 (1p36.12) and MYCL1 (1p34.1), and 1 each at D1S484 (1q24.1),IGF2R-3 (6q26), and TP53 (17p13.1) were used. LOH at D1S2843 and D1S513 was detected in HCCs (20.4% and 23.5%, respectively), HGDNs (7.7% and 18.5%), LGDNs (13.6% and 6.9%), and CNs surrounding either HCCs or DNs (7.4% and 8.3%). These results demonstrate that LOH at D1S2843 and D1S513 are early events in human liver carcinogenesis. Data from CN surrounding either HCCs or DN, and also nodule-in-nodule lesions, provide evidence supporting a CN --> DN --> HCC progression. Different deletion patterns from multiple HCCs and DNs suggest independent origins for carcinogenesis in the same individual.

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