Question

《怪物公司》主题曲if i didnt have you 的歌词是什么

Answer 1

If I Didn't Have You Lyrics

If I were a rich man
With a million or two
I'd live in a penthouse
In a room, with a view
And if I were handsome
(No way)
It could happen
Those dreams do come true
I wouldn't have nothin'
If I didn't have you
Wouldn't have nothin'
If I didn't have
Wouldn't have nothin'
If I didn't have
Wouldn't have nothin'
Can I tell you something?
For years I have envied
(You green with it)
Your grace and your charm
Everyone loves you, you know?
(Yes I know, I know, I know)
I must admit it
Big guy
You always come through
I wouldn't have nothin'
If I didn't have you
You and me together
That's how it
Always should be
One without the other
Don't mean nothing to me
Nothing to me
Ya
I wouldn't be nothin'
(Aw now)
If I didn't have you
To serve
I'm just
A punky little eyeball
And a funky optic nerve
Hey I never told you this
Sometimes
I get a little blue
(Looks good on you)
But I wouldn't have nothin'
If I didn't have you
Let's dance (haha)
Look Ma
I'm dancin'
Would you let me lead?
Look at
That it' two big guys
Who're light on their feet
Don't you dare dip me
Don't you dare dip me
Don't you dare dip me
Ow I should have stretched
Yes I wouldn't be nothin
If I didn't have you
(I know what you mean
Sulley because)
I wouldn't know
Where to go
(Me too because I)
Or know, what to do
(Why do you keep
Singin' my part)
I don't have to say it
(Aw say it anyway)
Cause we both know
It's true
I wouldn't have nothin'
If I didn't have
I wouldn't have nothin'
If I didn't have
I wouldn't have nothin'
If I didn't have
Wouldn't have nothin'
If I didn't have
Youuuuu
One more time, big one
Don't have to say it
Where'd everybody come from?
Oh, we both know it's true
Let's take it home big guy
I wouldn't have nothin'
If I didn't have
I wouldn't have nothin'
If I didn't have
I wouldn't have nothin'
If I didn't have
You, you, you
A-E-I-O
That means you
Ya

Answer 2

Polo-like kinase 1 (Plk1) is an important target for antineoplastic therapy because of its required functions in cell division, as well as the enhanced sensitivity of cancer cells to its inactivation. Several Plk1-targeted drugs have emerged, including BI-2536 and ZK-thiazolidinone (TAL). These inhibitors of Plk1 arrest cells in mitosis and evoke phenotypes consistent with downregulating Plk1 by other means.BI-2536 and a pharmacologically optimized analogue (BI-6727) have shown promising signs of activity in preliminary clinical trials. A chemical genetic system for inhibiting Plk1 has also been developed. In this system, both copies of the PLK1 locus were deleted from immortalized human retinal pigment epithelial cells through targeting and Cre-lox-mediated recombination. After Cre-mediated excision, PLK1–/– clones are inviable unless they are complemented by expression of Plk1 in trans, either wildtype (Plk1wt) or a compound mutant (L130G C67V; hereafter Plk1as). By enlarging the kinase’s active site, the latter mutations allow Plk1 to accept bulky purine analogues as ATP-competitive inhibitors. We report here that these mutations also have the unexpected effect of desensitizing Plk1 to clinically useful inhibitors such as BI-2536 and TAL. (Structures for all chemicals used are shown in Supplementary Figure 1.)
In the course of examining the anti-proliferative activity of BI-2536, we discovered that this compound strongly retarded the growth of Plk1wt cells but had little or no effect on Plk1as cells (Figure 1A,B). To determine if this change in inhibitor potency was unique to BI-2536, we performed similar growth-challenge experiments with TAL, a structurally distinct Plk1 inhibitor. Again, we observed a marked difference between Plk1as cells and their isogenic Plk1wt counterparts (Figure 1C,D). To understand the depth and breadth of inhibitor resistance, we queried multiple in vivo readouts of Plk1 activity. Plk1 is required throughout mitosis, with well-characterized roles in centrosome maturation, bipolar spindle assembly, stabilization of kinetochore-microtubule attachments, and initiation of cytokinesis. Each of these programs proved to be qualitatively and quantitatively resistant to both Plk1-targeted inhibitors. For instance, Plk1as cells continued to recruit γ-tubulin to centrosomes (a cardinal manifestation of centrosome maturation) and form bipolar spindles in the presence of BI-2536 (Figure 2A) and TAL (Figure 2B). Likewise, BubR1 hyper-phosphorylation by Plk1 (a crucial determinant of stable kinetochore-microtubule attachment) was undiminished, as reflected in the BubR1 polypeptide’s persistent mobility shift on SDS-PAGE (Figure 2C). Consistent with this broad array of defects, both compounds caused Plk1wt (but not Plk1as cells) to arrest in mitosis, as judged from their rounded appearance by phase-contrast microscopy (shown below in Figure 4).