anti-Four and A Half LIM Domains 1 (FHL1) Antibodies

Human Four and A Half LIM Domains 1 (FHL1) interaction partners

1. FHL1 increase inhibitory CDC25 phosphorylation by forming a complex with CHK2 and CDC25, and sequester CDC25 in the cytoplasm by forming another complex with 14-3-3 and CDC25, resulting in increased radioresistance in cancer cells.

2. FHL1 promote paclitaxel resistance in hepatocellular carcinomas cells through regulating apoptosis induced by paclitaxel, suggesting that FHL1 may be a promising molecular target for Hepatocellular carcinoma therapy.

3. Altogether, the specific localization of FHL1B and its modulation in disease-patient's myoblasts confirmed FHL1-related Emery-Dreifuss muscular dystrophy as a nuclear envelope disease.

4. Low FHL1 expression is associated with head and neck squamous cell carcinoma.

5. We have uncovered FHL1 as a novel potential regulator of calcium homeostasis in both fish and humans and have implicated it in isolated hypoparathyroidism.

6. Mutations in FHL1 cause unclassifiable cardiomyopathy with coexisting Emery-Dreifuss muscular dystrophy.

7. results provide evidence that FHL1A interacts with PLEKHG2 and regulates cell morphological change through the activity of PLEKHG2.

8. a novel FHL1 splice site variant results in the absence of FHL1A and the abundance of FHL1C, which may contribute to the complex and severe phenotype of Uruguay syndrome.

9. Knockdown of FHL1 with FHL1 small interfering RNA (siRNA) promoted tumor growth and Cyclin D and cyclin E were markedly elevated at both the protein and mRNA level.

10. results indicate that anti-FHL1 autoantibodies in peripheral blood have promising potential as a biomarker to identify a subset of severe IIM.

11. In healthy individuals, FHL1A is the predominant splice variant and is mainly found in skeletal and cardiac muscle. In two individuals with an Emery-Dreifuss plus phenotype with pulmonary artery hypoplasia and facial dysmorphology, there was demonstrated loss of isoform A and B, and an almost 200-fold overexpression of isoform C.

12. FRG1 mice overexpressing FHL1 showed an improvement in the dystrophic phenotype

13. FHL1 shRNA could significantly accelerate tumor cell growth via inhibiting the expression of FHL1

14. Our results suggest that miR-410 may function as an oncomiR and are consistent with its key function in regulating FHL1 in certain digestive system cancers.

15. These data suggested that up-regulated FHL1 in smooth muscle in HSCR might be associated with intestinal wall remodeling in HSCR and might be one of the risk factors for gastrointestinal motor dysfunction

16. This is the first study to show that FHL1 mutations identified in several clinically distinct myopathies lead to similar protein aggregation and impair myotube formation.

17. The study has revealed that FHL1C overexpression induces Jurkat cell apoptosis.

18. FHL-1 is the predominant complement regulator in Bruch's membrane having direct implications for age-related macular degeneration.

19. Data indicate that four-and-a-half LIM domain 1 gene FHL1 mutation causing isolated hypertrophic cardiomyopathy with X-chromosomal inheritance.

20. Data show that loss of FHL1 function leads to myopathy in vivo and suggest that loss of function of FHL1 may be one of the mechanisms underlying muscle dystrophy in patients with FHL1 mutations.

Mouse (Murine) Four and A Half LIM Domains 1 (FHL1) interaction partners

1. KyoT2 downregulates airway remodeling and resistance in asthmatic mice through a Hes1-dependent mechanism.

2. Results found that osteogenesis increases with the overexpression of Fhl1 and decreases with reduced Fhl1 expression and suggest that Fhl1 mediates interacting estrogen and Wnt signaling during osteogenesis.

3. Findings indicate that loss of function is responsible for the myopathy in the Fhl1 W122S knock-in mice.

4. The CSL-KyoT2 corepressor complex is a negative regulator of Notch signaling.

5. Data show that loss of FHL1 function leads to myopathy in vivo and suggest that loss of function of FHL1 may be one of the mechanisms underlying muscle dystrophy in patients with FHL1 mutations.

6. Fhl1 transcriptional changes provide salutary effects on stressed myocytes in cardiomyopathy.

7. Data suggest Fhl1 (four-and-a-half LIM domains protein 1) and FHL2 (four-and-a-half LIM domains protein 2) bind to and regulate activity of Prkd1 (protein kinase D 1) in cardiac/ventricular myocytes; knockdown of Fhl1 down-regulates Prkd1 activation.

8. A novel mechanism involving four-and-a-half LIM domain protein-1 and extracellular signal-regulated kinase-2 regulates titin phosphorylation and mechanics.

9. Wnt signaling induces muscle cell differentiation, at least partly, through Fhl1 activation.

10. FHL1 is a novel regulator of myosin-binding protein C activity that may have a role in sarcomere assembly

11. These results suggest that KyoT2 is a substrate of SUMO modification catalyzed by PIAS1, and that SUMOylation may modulate the transcriptional repression effect of KyoT2 on the Notch/RBP-J signaling pathway.

12. significantly altered expression after short-term hypoxic exposure; identified as a novel protein regulated in various forms of pulmonary hypertension

13. KyoT3 is an isoform of murine FHL1, which associates with the transcription factor RBP-J and represses the RBP-J-mediated transactivation

14. four-and-a-half LIM domains 1 (FHL1) is part of a complex within the cardiomyocyte sarcomere that senses the biomechanical stress-induced responses important for cardiac hypertrophy.

15. FHL1 appears to modulate muscle mass and strength enhancement.

16. Data show that SLIMMER delayed Siva-1-dependent apoptosis in C2C12 myoblasts.

Pig (Porcine) Four and A Half LIM Domains 1 (FHL1) interaction partners

1. The LIM domain protein FHL1C interacts with tight junction protein ZO-1 contributing to the epithelial-mesenchymal transition of a breast adenocarcinoma cell line.