Transglutaminase 3 (E Polypeptide, Protein-Glutamine-gamma-Glutamyltransferase) Protéines (TGM3)

Human Transglutaminase 3 (E Polypeptide, Protein-Glutamine-gamma-Glutamyltransferase) (TGM3) interaction partners

1. aberrant TGase 1 and TGase 3 localization and distribution are closely related to hyper-keratinization in Oral lichen planus.

2. Patents having higher level of TGM-3 expression have good response to chemo-radiotherapy and also have better overall survival. TGM-3 may serve as a candidate biomarker for responsiveness to chemo-radiotherapy treatment in oral squamous cell carcinoma patients

3. Cultured duodenal biopsies from patients with dermatitis herpetiformis produce transglutaminase-3 antibodies.

4. Levels of TG3-IgA IC significantly elevated in plasma as well as in serum samples of untreated patients with dermatitis herpetiformis compared with healthy controls.

5. studies demonstrate that TGase-catalyzed transamidation and activation of rac1 and cdc42 results from stimulation of multiple types of receptors and this novel signaling pathway can regulate dendritic spine morphology and plasticity.

6. The two enzymes PADI3 and TGM3, responsible for posttranslational protein modifications, and their target structural protein TCHH are all involved in hair shaft formation.

7. Data indicate a decrease in transglutaminases TG1 and TG3 transcripts by about 70% in foreskins from patients with balanitis xerotica obliterans (BXO) BXO in comparison with patients without BXO and an increase in transglutaminase TG2 mRNA levels by 2.9 fold.

8. Our data collectively demonstrate that TGM3 can be a candidate tumor suppressor that is able to induce esophageal cancer cell proliferation and migration

9. mRNA expression of transglutaminase 1 and transglutaminase 3 was significantly decreased in patients with chronic periodontitis compared with a healthy control group.

10. Transglutaminase 3 present in the IgA aggregates in dermatitis herpetiformis skin is enzymatically active and binds soluble fibrinogen.

11. New basal cell carcinoma susceptibility loci were identified at TGM3 (rs214782) and RGS22(rs7006527).

12. IgA-anti-TG1 antibodies were found in 2% and IgA-anti-TG3 antibodies in 3% of patients with active atopic dermatitis (AD). Two out of the 5 patients with AD and concomitant celiac disease had IgA-anti-TG1 and IgA-anti-TG2 antibodies.

13. TGM3, a candidate tumor suppressor, contributes to the carcinogenesis and development of human head and neck cancer.

14. Genetic variation in the epidermal transglutaminase genes is not associated with atopic dermatitis.

15. The low expression of TGM3 may contribute to the carcinogenesis and development of laryngeal carcinoma.

16. TGM3 in immunoglobulin A (IgA) and TGM3 immune complexes is responsible for cross-linking and tight binding of IgA to connective tissue in the dermis and explains the IgA deposits in dermatitis herpetiformis skin long after signs of disease are resolved.

17. findings lend credence to the notion that TG3 and TG6 are involved in the gluten-induced autoimmune responses of dermatitis herpetiformis and gluten ataxia

18. new information on the specific distribution of TGase 3

19. epidermal transglutaminase (type 3) is the dominant autoantigen in dermatitis herpetiformis

20. x-ray crystallography in the presence of Ca2+ and/or Mg+2 shows Ca2+ binding in both sites two and three cooperate in opening the channel

Mouse (Murine) Transglutaminase 3 (E Polypeptide, Protein-Glutamine-gamma-Glutamyltransferase) (TGM3) interaction partners

1. study concludes that the classic wellhaarig mutations result from defects in Tgm3

2. The mutant gene we is probably responsible for a disrupted induction signal from the dermal papilla towards ectodermal cells of a hair follicle.

3. The first signs of alopecia in mice of the +/Fgf5(go-Y) we/wewal/wal genotype appear only three days later than in double +/+ we/wewal/wal homozygotes.

4. Fluctuations of BMP2 signaling pathway during hair cycles in skin with mutant genes we, wal and Fgf5(go).

5. Interaction of mutant genes Fgf5(go-Y), we, and wal changes the duration of hair growth cycles in mice

6. The clinically uninvolved skin in TGM3 knockout mice showed impaired barrier function and higher susceptibility to FITC sensitization indicating that TGM3 has a significant contribution to the functionally intact cutaneous barrier.

7. Loss of Tgm3 is associated with defective hair development.

8. new information on the specific distribution of TGase 3

9. N-terminus sequence of the proteolyzed fragment was analyzed with specific antibodies.

10. The expression of TGM3 may play a important role in the epidermis differentiation in embryogenesis.

11. detected two splicing variants for TG3, as the transcription of these mRNAs appears to be not regulated during differentiation and in pathologies involving tranglutaminase activity