PMID- 35148273
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220329
IS  - 2049-3614 (Print)
IS  - 2049-3614 (Electronic)
IS  - 2049-3614 (Linking)
VI  - 11
IP  - 3
DP  - 2022 Mar 14
TI  - The role of menin in bone pathology.
LID - 10.1530/EC-21-0494 [doi]
LID - e210494
AB  - Multiple endocrine neoplasia type 1 (MEN1) is the most common cause of hereditary 
      primary hyperparathyroidism (PHPT). Bone disorders are considered one of the key 
      symptoms in PHPT present with the significant reduction in bone mineral density 
      and low-energy fractures. Previously, these bone disorders were believed to be 
      caused solely by the increase in the level of parathyroid hormone and its 
      subsequent effect on bone resorption. The current paradigm, however, states that 
      the mutations in the menin gene, which cause the development of MEN1, can also 
      affect the metabolism of the cells of the osteoid lineage. This review analyzes 
      both the proven and the potential intracellular mechanisms through which menin 
      can affect bone metabolism.
FAU - Gorbacheva, Anna
AU  - Gorbacheva A
AUID- ORCID: 0000-0003-2669-9457
AD  - Endocrinology Research Center, Moscow, Russian Federation.
FAU - Eremkina, Anna
AU  - Eremkina A
AUID- ORCID: 0000-0001-6667-062X
AD  - Endocrinology Research Center, Moscow, Russian Federation.
FAU - Goliusova, Daria
AU  - Goliusova D
AD  - Endocrinology Research Center, Moscow, Russian Federation.
FAU - Krupinova, Julia
AU  - Krupinova J
AD  - Endocrinology Research Center, Moscow, Russian Federation.
FAU - Mokrysheva, Natalia
AU  - Mokrysheva N
AD  - Endocrinology Research Center, Moscow, Russian Federation.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20220314
PL  - England
TA  - Endocr Connect
JT  - Endocrine connections
JID - 101598413
PMC - PMC8942318
OTO - NOTNLM
OT  - men 1 protein
OT  - menin
OT  - multiple endocrine neoplasia type 1
OT  - osteoporosis
EDAT- 2022/02/12 06:00
MHDA- 2022/02/12 06:01
PMCR- 2022/02/11
CRDT- 2022/02/11 17:11
PHST- 2022/01/17 00:00 [received]
PHST- 2022/02/11 00:00 [accepted]
PHST- 2022/02/12 06:00 [pubmed]
PHST- 2022/02/12 06:01 [medline]
PHST- 2022/02/11 17:11 [entrez]
PHST- 2022/02/11 00:00 [pmc-release]
AID - EC-21-0494.R2 [pii]
AID - EC-21-0494 [pii]
AID - 10.1530/EC-21-0494 [doi]
PST - epublish
SO  - Endocr Connect. 2022 Mar 14;11(3):e210494. doi: 10.1530/EC-21-0494.