α-Actinin-3 deficiency is associated with reduced bone mass in human and mouse (Q24316366)

GOA release 2020-03-11

5

Peter J Houweling

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Kathryn North

21

object named as

Kathryn N North

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John A Eisman

14

object named as

John A Eisman

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Jacqueline R. Center

16

object named as

Jacqueline R Center

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author name string

Nan Yang

1

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Aaron Schindeler

2

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Michelle M McDonald

3

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Jane T Seto

4

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Monkol Lek

6

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Marshall Hogarth

7

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Alyson R Morse

8

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Joanna M Raftery

9

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Dominic Balasuriya

10

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Daniel G MacArthur

11

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Yemima Berman

12

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Kate G R Quinlan

13

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Tuan V Nguyen

15

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Richard L Prince

17

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Scott G Wilson

18

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Kathy Zhu

19

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David G Little

Effects of calcium supplementation on clinical fracture and bone structure: results of a 5-year, double-blind, placebo-controlled trial in elderly women.

20

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language of work or name

English

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publication date

October 2011

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published in

Bone

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volume

49

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issue

4

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page(s)

790-8

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cites work

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A common nonsense mutation results in alpha-actinin-3 deficiency in the general population.

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Loss of ACTN3 gene function alters mouse muscle metabolism and shows evidence of positive selection in humans

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Mdm2 is involved in the ubiquitination and degradation of G-protein-coupled receptor kinase 2

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ACTN3 polymorphism affects thigh muscle area

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α-Actinin-3 deficiency results in reduced glycogen phosphorylase activity and altered calcium handling in skeletal muscle

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Disruption of alpha-actinin-integrin interactions at focal adhesions renders osteoblasts susceptible to apoptosis

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A gene for speed: contractile properties of isolated whole EDL muscle from an alpha-actinin-3 knockout mouse

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Mechanical loading by fluid shear is sufficient to alter the cytoskeletal composition of osteoblastic cells

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ACTN3 genotype is associated with muscle phenotypes in women across the adult age span

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