anti-Motor Neuron and Pancreas Homeobox 1 (MNX1) Antibodies

Human Motor Neuron and Pancreas Homeobox 1 (MNX1) interaction partners

1. MNX1-AS1 promoted the proliferation, migration, and invasion of GBM cells through inhibiting miR-4443.

2. MNX1 may directly regulate TrkB expression, which may increase their metastatic potential via suppression of anoikis and enhanced adhesion to the ECM.

3. Pathogenic variants in MNX1 were detected in 28% of all CS cases and 25% of sporadic cases. The clinical phenotype was variable in patients with and without pathogenic variants; no significant genotype-phenotype correlation was observed.

4. Findings identify RGS12 as a candidate tumor-suppressor gene in AA prostate cancer, which acts by decreasing expression of AKT and MNX1, establishing a novel oncogenic axis in this disparate disease setting.

5. MNX1 as a novel targetable oncogene increased in African-American (AA) prostate cancer that is associated with aggressive disease.

6. Findings demonstrated for the first time that lncRNA MNX1-AS1 functions as an oncogene in ovarian cancer.

7. The results illustrated miR-200a and miR-141 could inhibit the expression of Hlxb9 by binding to its mRNA 3'UTR. Furthermore, the expression of miR-200a and miR-141 was almost reciprocal to that of Hlxb9. Overexpression of miR-200a and miR-141 downregulated the expression of pancreatic progenitor cell markers Hlxb9

8. The nuclear positioning of the HLXB9 gene was monitored at different stages.

9. study reports the results of MNX1 mutational screening in a series of 28 cases suspected having Currarino Syndrome and characterization of 10 novel mutations

10. NKX2-2 and MNX1 are etiological genes for neonatal diabetes.

11. Both pHLXB9 and active GSK-3beta are elevated in beta cells with menin knockdown, in MEN1-associated beta cell tumors (insulinomas)

12. study describes a Norwegian family with typical Currarino syndrome in which a heterozygous deletion removes the entire MNX1 gene but no other known genes; also report MNX1 mutations in 3other Norwegian families and confirm that the GCC12 repeat (c.373_375[12]) is a normal allelic variant

13. HB9 binds to the prostaglandin E receptor 2 promoter and inhibits intracellular cAMP mobilization in leukemic cells.

14. a new HLXB9 gene mutation identified in a Chinese family with members suffering from Currarino syndrome

15. two novel mutations in the MNX1 gene in cases with Currarino syndrome

16. 2 previously described mutations, 1 de novo nonsense mutation (p.Gln212X) & 1 maternally inherited frameshift mutation (p.Pro18ProfsX38)were found among 14 Currarino syndrome patients with presacral tumors.

17. Hypermethylation of HLXB9 results in loss of expression and is associated with acute lymphoblastic leukemia.

18. HLXB9 is overexpressed in patients with infantile acute myeloid leukemia.

19. Incomeplete Curarino syndrome with more advantageous prognosis with autosomal domiant pattern homebox gene HLXBV9 mutation.

20. study reports on the MNX1 mutations in a family segregating Currarino syndrome (CS) & 3 sporadic CS patients & on clinical characteristics of the affected individuals

Mouse (Murine) Motor Neuron and Pancreas Homeobox 1 (MNX1) interaction partners

1. excitatory Hb9::Cre-derived interneurons constitute a distinct population of neurons that participates in the rhythm generating kernel for spinal locomotion.

2. Inactivating Mnx1 in embryonic beta-cells (Mnx1(Deltabeta)) caused beta-to-delta-like cell transdifferentiation, which was delayed until postnatal stages; findings identify Mnx1 as an important factor in beta-cell differentiation and proliferation.

3. provide mechanistic insights into the role of phospho-HLXB9 as a pro-oncogenic factor by interacting with a survival factor and by promoting the oncogenic c-Met pathway

4. NKX2-2 and MNX1 are etiological genes for neonatal diabetes.

5. Both pHLXB9 and active GSK-3beta are elevated in beta cells with menin knockdown, in MEN1-associated beta cell tumors (insulinomas)

6. Hlxb9 expression is increased in mouse islet tumor.

7. we developed recombinant lentiviral vectors carrying motor neuron specific regulatory sequences derived from the promoter of homeobox gene Hb9

8. Mnx1, a gene that is absolutely required in pancreas progenitors, is a major direct target of Ptf1a and is regulated by a distant enhancer element.

9. This study suggested that Hb9 interneurons are part of the sensorimotor circuitry that regulates the pattern of locomotor rhythms in the isolated cord.

10. the molecular pathways regulating Hb9 expression are evolutionarily conserved, and that MN-specific gene expression may be directed and achieved using a small 125-bp 5' enhancer

11. Hb9+ interneurons exhibit strong postinhibitory rebound and demonstrate pronounced membrane potential oscillations in response to chemical stimuli that induce locomotor activity.

12. Hb9 interneurons are both endogenous bursters and rhythmically active within a heterogeneous electrotonically coupled network

13. Hlxb9 and Tcfap2b were identified as genes whose expression was elevated in the ZPA compared to the rest of the developing limb bud.

Zebrafish Motor Neuron and Pancreas Homeobox 1 (MNX1) interaction partners

1. loss of Pax6b or Hb9 independently results in the loss of insulin expression, the data reveal a novel cross-talk between the two essential regulators of early beta-cell differentiation.

2. These data confirm our previous findings that Mnx1 is important for beta cell fates both in dorsal and ventral bud-derived beta cells.

3. This study demonistrated that Zebrafish Mnx proteins specify one motoneuron subtype and suppress acquisition of interneuron characteristics.

4. Data suggest that Mnx1 functions to promote beta and suppress alpha cell fates in the developing pancreas.

5. Essential for differentiation of the insulin-producing beta-cells but not morphogenesis of pancreas.