Connection

WEIMIN BI to Mice

This is a "connection" page, showing publications WEIMIN BI has written about Mice.
Connection Strength

0.149
  1. Increased LIS1 expression affects human and mouse brain development. Nat Genet. 2009 Feb; 41(2):168-77.
    View in: PubMed
    Score: 0.024
  2. Rai1 deficiency in mice causes learning impairment and motor dysfunction, whereas Rai1 heterozygous mice display minimal behavioral phenotypes. Hum Mol Genet. 2007 Aug 01; 16(15):1802-13.
    View in: PubMed
    Score: 0.022
  3. Inactivation of Rai1 in mice recapitulates phenotypes observed in chromosome engineered mouse models for Smith-Magenis syndrome. Hum Mol Genet. 2005 Apr 15; 14(8):983-95.
    View in: PubMed
    Score: 0.018
  4. Genes in a refined Smith-Magenis syndrome critical deletion interval on chromosome 17p11.2 and the syntenic region of the mouse. Genome Res. 2002 May; 12(5):713-28.
    View in: PubMed
    Score: 0.015
  5. LMOD2-related dilated cardiomyopathy presenting in late infancy. Am J Med Genet A. 2022 06; 188(6):1858-1862.
    View in: PubMed
    Score: 0.015
  6. Bi-allelic Variants in TONSL Cause SPONASTRIME Dysplasia and a Spectrum of Skeletal Dysplasia Phenotypes. Am J Hum Genet. 2019 03 07; 104(3):422-438.
    View in: PubMed
    Score: 0.012
  7. Biallelic Variants in OTUD6B Cause an Intellectual Disability Syndrome Associated with Seizures and Dysmorphic Features. Am J Hum Genet. 2017 Apr 06; 100(4):676-688.
    View in: PubMed
    Score: 0.011
  8. A duplication CNV that conveys traits reciprocal to metabolic syndrome and protects against diet-induced obesity in mice and men. PLoS Genet. 2012; 8(5):e1002713.
    View in: PubMed
    Score: 0.008
  9. Penetrance of craniofacial anomalies in mouse models of Smith-Magenis syndrome is modified by genomic sequence surrounding Rai1: not all null alleles are alike. Am J Hum Genet. 2007 Mar; 80(3):518-25.
    View in: PubMed
    Score: 0.005
  10. Rai1 duplication causes physical and behavioral phenotypes in a mouse model of dup(17)(p11.2p11.2). J Clin Invest. 2006 Nov; 116(11):3035-41.
    View in: PubMed
    Score: 0.005
  11. Phenotypic characterization of Bbs4 null mice reveals age-dependent penetrance and variable expressivity. Hum Genet. 2006 Sep; 120(2):211-26.
    View in: PubMed
    Score: 0.005
  12. Reduced penetrance of craniofacial anomalies as a function of deletion size and genetic background in a chromosome engineered partial mouse model for Smith-Magenis syndrome. Hum Mol Genet. 2004 Nov 01; 13(21):2613-24.
    View in: PubMed
    Score: 0.004
  13. Modeling del(17)(p11.2p11.2) and dup(17)(p11.2p11.2) contiguous gene syndromes by chromosome engineering in mice: phenotypic consequences of gene dosage imbalance. Mol Cell Biol. 2003 May; 23(10):3646-55.
    View in: PubMed
    Score: 0.004
Connection Strength

The connection strength for concepts is the sum of the scores for each matching publication.

Publication scores are based on many factors, including how long ago they were written and whether the person is a first or senior author.