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SALL1
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Sal-like protein 1 (Spalt-like transcription factor 1) (Zinc finger protein 794) (Zinc finger protein SALL1) (Zinc finger protein Spalt-1) (HSal1) (Sal-1) [SAL1] [ZNF794] ==Publications== {{medline-entry |title=[[SALL1]] functions as a tumor suppressor in breast cancer by regulating cancer cell senescence and metastasis through the NuRD complex. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29625565 |abstract=[[SALL1]] is a multi-zinc finger transcription factor that regulates organogenesis and stem cell development, but the role of [[SALL1]] in tumor biology and tumorigenesis remains largely unknown. We analyzed [[SALL1]] expression levels in human and murine breast cancer cells as well as cancer tissues from different types of breast cancer patients. Using both in vitro co-culture system and in vivo breast tumor models, we investigated how [[SALL1]] expression in breast cancer cells affects tumor cell growth and proliferation, metastasis, and cell fate. Using the gain-of function and loss-of-function strategies, we dissected the molecular mechanism responsible for [[SALL1]] tumor suppressor functions. We demonstrated that [[SALL1]] functions as a tumor suppressor in breast cancer, which is significantly down-regulated in the basal like breast cancer and in estrogen receptor (ER), progesterone receptor (PR) and epidermal growth factor receptor 2 (HER2) triple negative breast cancer patients. [[SALL1]] expression in human and murine breast cancer cells inhibited cancer cell growth and proliferation, metastasis, and promoted cell cycle arrest. Knockdown of [[SALL1]] in breast cancer cells promoted cancer cell growth, proliferation, and colony formation. Our studies revealed that tumor suppression was mediated by recruitment of the Nucleosome Remodeling and Deacetylase (NuRD) complex by [[SALL1]], which promoted cancer cell senescence. We further demonstrated that the mechanism of inhibition of breast cancer cell growth and invasion by [[SALL1]]-NuRD depends on the p38 MAPK, ERK1/2, and mTOR signaling pathways. Our studies indicate that the developmental control gene [[SALL1]] plays a critical role in tumor suppression by recruiting the NuRD complex and thereby inducing cell senescence in breast cancer cells. |mesh-terms=* Animals * Cell Line, Tumor * Cell Proliferation * Cellular Senescence * Coculture Techniques * Down-Regulation * Female * Gene Expression Regulation, Neoplastic * Humans * MCF-7 Cells * Mi-2 Nucleosome Remodeling and Deacetylase Complex * Mice * Neoplasm Metastasis * Neoplasm Transplantation * Transcription Factors * Triple Negative Breast Neoplasms |keywords=* Breast cancer * Metastasis * NuRD complex * SALL1 * Senescence * Tumor suppressor gene * Tumorigenesis |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5889587 }} {{medline-entry |title=Genome-Wide Association Analysis of the Sense of Smell in U.S. Older Adults: Identification of Novel Risk Loci in African-Americans and European-Americans. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27878761 |abstract=The human sense of smell decreases with age, and a poor sense of smell are among the most important prodromal symptoms of several neurodegenerative diseases. Recent evidence further suggests a racial difference in the sense of smell among U.S. older adults. However, no genome-wide association study (GWAS) on the sense of smell has been conducted in African-Americans (AAs). We performed the first genome-wide meta-analysis of the sense of smell among 1979 AAs and 6582 European-Americans (EAs) from three U.S. aging cohorts. In the AA population, we identified nine novel regions (KLF4-[[ACTL7B]], [[RAPGEF2]]-[[FSTL5]], [[TCF4]]-LOC100505474, [[PCDH10]], KIAA1751, [[MYO5B]], MIR320B1-[[CD2]], [[NR5A2]]-[[LINC00862]], [[SALL1]]-C16orf97) that were associated with the sense of smell (P < 5 × 10 ). Many of these regions have been previously linked to neuropsychiatric (schizophrenia or epilepsy) or neurodegenerative (Parkinson's or Alzheimer's disease) diseases associated with a decreased sense of smell. In the EA population, we identified two novel loci in or near [[RASGRP1]] and ANXA2P3 associated with sense of smell. In conclusion, this study identified several ancestry-specific loci that are associated with the sense of smell in older adults. While these findings need independent confirmation, they may lead to novel insights into the biology of the sense of smell in older adults and its relationships to neuropsychological and neurodegenerative diseases. |mesh-terms=* African Americans * Aged * Aging * European Continental Ancestry Group * Female * Genetic Predisposition to Disease * Genome-Wide Association Study * Genotype * Humans * Male * Polymorphism, Single Nucleotide * Risk * Smell * United States |keywords=* African-American * GWAS * The sense of smell |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5441979 }}
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