Connection

WEIMIN BI to Mice, Inbred C57BL

This is a "connection" page, showing publications WEIMIN BI has written about Mice, Inbred C57BL.
Connection Strength

0.076
  1. 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: 0.034
  2. 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: 0.012
  3. 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: 0.008
  4. 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: 0.008
  5. 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: 0.007
  6. 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: 0.006
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.